ORIGINAL_ARTICLE
A new insight into viral proteins as Immunomodulatory therapeutic agents. KSHV vOX2 a homolog of human CD200 as a potent anti-inflammatory protein
The physiologic function of the immune system is defense against infectious microbes and internal tumour cells, Therefore, need to have precise modulatory mechanisms to maintain the body homeostasis. The mammalian cellular CD200 (OX2)/CD200R interaction is one of such modulatory mechanisms in which myeloid and lymphoid cells are regulated. CD200 and CD200R molecules are membrane proteins that their immunomodulatory effects are able to suppress inflammatory responses, particularly in the privilege sites such as CNS and eyes. Kaposi’s sarcoma-associated herpesvirus (KSHV), encodes a wide variety of immunoregulatory proteins which play central roles in modulating inflammatory and anti-inflammatory responses in favour of virus dissemination. One such protein is a homologue of the, encoded by open reading frame (ORF) K14 and therefore called vOX2. Based on its gene expression profile during the KSHV life cycle, it is hypothesised that vOX2 modulates host inflammatory responses. Moreover, it seems that vOX2 involves in cell adhesion and modulates innate immunity and promotes Th2 immune responses. In this review the activities of mammalian CD200 and KSHV CD200 in cell adhesion and immune system modulation are reviewed in the context of potential therapeutic agents.
https://ijbms.mums.ac.ir/article_6408_620ebdfdfb45f513ce17002304ff0b9c.pdf
2016-01-01
2
13
10.22038/ijbms.2016.6408
CD200
Immune modulation
KSHV
RGD
vCD200
vOX2
Maryam
Mousavinezhad-Moghaddam
1
Department of Physiology, Biology Division, Faculty of Sciences, Ferdowsi University of Mashhad, Mashhad, Iran
AUTHOR
Abbas Ali
Amin
2
Department of Immunology, Faculty of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran
AUTHOR
Houshang
Rafatpanah
hrafatpanah@hotmail.com
3
Immunology Research Centre, Bu-Ali Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Seyed Abdol
Rahim Rezaee
rezaeer@mums
4
Inflammation and Inflammatory Diseases Research Center, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
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ORIGINAL_ARTICLE
Chemically primed bone-marrow derived mesenchymal stem cells show enhanced expression of chemokine receptors contributed to their migration capability
Objective(s):The limited homing potential of bone-marrow-derived mesenchymal stem cells (BM-MSC) is the key obstacle in MSC-based therapy. It is believed that chemokines and chemokine receptor interactions play key roles in cellular processes associated with migration. Meanwhile, MSCs express a low level of distinct chemokine receptors and they even lose these receptors on their surface after a few passages which influence their therapeutic applications negatively. This study investigated whether treatment of BM-MSCs with hypoxia-mimicking agents would increase expression of some chemokine receptors and cell migration. Materials and Methods: BM-MSCs were treated at passage 2 for our gene expression profiling. All qPCR experiments were performed by SYBR Green method in CFX-96 Bio-Rad Real-Time PCR. The Boyden chamber assay was utilized to investigate BM-MSC homing. Results:Possible approaches to increasing the expression level of chemokine receptors by different hypoxia-mimicking agents such as valproic acid (VPA), CoCl2, and desferrioxamine (DFX) are described. Results show DFX efficiently up-regulate the CXCR7 and CXCR4 gene expression while VPA increase only the CXCR7 gene expression and no significant change in expression level of CXCR4 and the CXCR7 gene was detectable by CoCl2 treatment. Chemotaxis assay results show that pre-treatment with DFX, VPA, and Cocl2 enhances significantly the migration ability of BM-MSCs compared with the untreated control group and DFX treatment accelerates MSCs homing significantly with a higher rate than VPA and Cocl2 treatments. Conclusion: Our data supports the notion that pretreatment of MSC with VPA and DFX improves the efficiency of MSC therapy by triggering homing regulatory signaling pathways.
https://ijbms.mums.ac.ir/article_6409_eace9d6f07c7fd009845ce6e5b4fe7ab.pdf
2016-01-01
14
19
10.22038/ijbms.2016.6409
CXCR4
CXCR7
CoCl2
Desferrioxamine
MSC
Chemical treatment
Homing
Valproic acid
Hamid Reza
Bidkhori
hbidkhori@gmail.com
1
Department of Biology, Faculty of Sciences, Ferdowsi University of Mashhad, Mashhad, Iran
AUTHOR
Naghmeh
Ahmadiankia
f.kalalian@gmail.com
2
Shahroud University of Medical Sciences, Shahroud, Iran
AUTHOR
Maryam
Moghaddam Matin
matin@um.ac.ir
3
Department of Biology, Faculty of Sciences, Ferdowsi University of Mashhad, Mashhad, Iran
AUTHOR
Asieh
Heirani tabasi
4
Department of Biology, Faculty of Sciences, Ferdowsi University of Mashhad, Mashhad, Iran
AUTHOR
Moein
Farshchian
moeinfarshchy@yahoo.com
5
Department of Biology, Faculty of Sciences, Ferdowsi University of Mashhad, Mashhad, Iran
AUTHOR
Hojjat
Naderi-meshkin
nahojjat@gmail.com
6
Stem Cells and Regenerative Medicine Research Department, ACECR-Khorasan Razavi Branch, Mashhad, Iran
AUTHOR
Mina
Shahriyari
m.shahriyari@outlook.com
7
Stem Cells and Regenerative Medicine Research Department, ACECR-Khorasan Razavi Branch, Mashhad, Iran
AUTHOR
Mahtab
Dastpak
ma.dastpak@gmail.com
8
Department of Biology, Faculty of Sciences, Ferdowsi University of Mashhad, Mashhad, Iran
AUTHOR
Ahmad Reza
Bahrami
ar-bahram@um.ac.ir
9
Department of Biology, Faculty of Sciences, Ferdowsi University of Mashhad, Mashhad, Iran
LEAD_AUTHOR
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6. Naderi-Meshkin H, Matin MM, Heirani-Tabasi A, Mirahmadi M, Irfan-Maqsood M, Edalatmanesh MA, et al. Injectable hydrogel delivery plus preconditioning of mesenchymal stem cells: exploitation of SDF-1/CXCR4 axis towards enhancing the efficacy of stem cells' homing. Cell Biol Int 2015: doi: 10.1002/cbin.10474. [Epub ahead of print]
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7. Naderi-Meshkin H, Bahrami AR, Bidkhori HR, Mirahmadi M, Ahmadiankia N. Strategies to improve homing of mesenchymal stem cells for greater efficacy in stem cell therapy. Cell Biol Int 2015; 39:23-34. 8. Tsai LK, Leng Y, Wang Z, Leeds P, Chuang DM. The mood stabilizers valproic acid and lithium enhance mesenchymal stem cell migration via distinct mechanisms. Neuropsychopharmacology 2010; 35:2225-2237.
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9. Li L, Yin X, Ma N, Lin F, Kong X, Chi J, et al. Desferrioxamine regulates HIF-1 alpha expression in neonatal rat brain after hypoxia-ischemia. Am J Translat Res 2014; 6:377-383.
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12. da Silva Meirelles L, Caplan AI, Nardi NB. In search of the in vivo identity of mesenchymal stem cells. Stem Cells 2008; 26:2287-2299.
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13. Ahmadian Kia N, Bahrami AR, Ebrahimi M, Matin MM, Neshati Z, Almohaddesin MR, et al. Comparative analysis of chemokine receptor's expression in mesenchymal stem cells derived from human bone marrow and adipose tissue. J Mol Neurosci 2011; 44:178-185.
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14. Ganju RK, Brubaker SA, Meyer J, Dutt P, Yang Y, Qin S, et al. The alpha-chemokine, stromal cell-derived factor-1alpha, binds to the transmembrane G-protein-coupled CXCR-4 receptor and activates multiple signal transduction pathways. J Biol chem 1998; 273:23169-23175.
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15. De Clercq E. The bicyclam AMD3100 story. Nat Rev Drug Discov 2003; 2:581-587.
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16. Tsai LK, Wang Z, Munasinghe J, Leng Y, Leeds P, Chuang DM. Mesenchymal stem cells primed with valproate and lithium robustly migrate to infarcted regions and facilitate recovery in a stroke model. Stroke 2011; 42:2932-2939.
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17. Jeon ES, Shin JH, Hwang SJ, Moon GJ, Bang OY, Kim HH. Cobalt chloride induces neuronal differentiation of human mesenchymal stem cells through upregulation of microRNA-124a. Biochem Biophys Res Commun 2014; 444:581-587.
16
18. McDermott DH, Lopez J, Deng F, Liu Q, Ojode T, Chen H, et al. AMD3100 is a potent antagonist at CXCR4(R334X) , a hyperfunctional mutant chemokine receptor and cause of WHIM syndrome. J Cell Mol Med 2011; 15:2071-2081.
17
19. Won YW, Patel AN, Bull DA. Cell surface engineering to enhance mesenchymal stem cell migration toward an SDF-1 gradient. Biomaterials 2014; 35):5627-5635.
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20. Sarkar D, Zhao W, Gupta A, Loh WL, Karnik R, Karp JM. Cell surface engineering of mesenchymal stem cells. Methods Mol Biol 2011; 698:505-523.
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21. Sarkar D, Spencer JA, Phillips JA, Zhao W, Schafer S, Spelke DP, et al. Engineered cell homing. Blood 2011; 118:e184-191.
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22. Mazzinghi B, Ronconi E, Lazzeri E, Sagrinati C, Ballerini L, Angelotti ML, et al. Essential but differential role for CXCR4 and CXCR7 in the therapeutic homing of human renal progenitor cells. J Exp Med 2008; 205:479-490.
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23.Najafi R, Sharifi AM. Deferoxamine preconditioning potentiates mesenchymal stem cell homing in vitro and in streptozotocin-diabetic rats. Expert Opin Biol Ther 2013; 13:959-972.
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24. Zabel BA, Wang Y, Lewen S, Berahovich RD, Penfold ME, Zhang P, et al. Elucidation of CXCR7-mediated signaling events and inhibition of CXCR4-mediated tumor cell transendothelial migration by CXCR7 ligands. J Immunol 2009; 183:3204-3211.
23
25. Gul H, Marquez-Curtis LA, Jahroudi N, Larratt LM, Janowska-Wieczorek A. Valproic acid exerts differential effects on CXCR4 expression in leukemic cells. Leuk Res 2010; 34:235-242.
24
26. Cho GW, Kang BY, Kim KS, Kim SH. Effects of valproic acid on the expression of trophic factors in human bone marrow mesenchymal stromal cells. Neurosci Lett 2012; 526:100-105.
25
27. Jeong SG, Ohn T, Kim SH, Cho GW. Valproic acid promotes neuronal differentiation by induction of neuroprogenitors in human bone-marrow mesenchymal stromal cells. Neurosci Lett 2013; 554:22-27.
26
ORIGINAL_ARTICLE
Conjugated linoleic acid supplementation enhances insulin sensitivity and peroxisome proliferator-activated receptor gamma and glucose transporter type 4 protein expression in the skeletal muscles of rats during endurance exercise
Objective(s):This study examined whether conjugated linoleic acid (CLA) supplementation affects insulin sensitivity and peroxisome proliferator-activated receptor gamma (PPAR-γ) and glucose transporter type 4 (GLUT-4) protein expressions in the skeletal muscles of rats during endurance exercise.
Materials and Methods:Sprague-Dawley male rats were randomly divided into HS (high-fat diet (HFD) sedentary group, n = 8), CS (1.0% CLA supplemented HFD sedentary group, n = 8), and CE (1.0% CLA supplemented HFD exercise group, n = 8). The rats in the CE swam for 60 min a day, 5 days a week for 8 weeks.
Results:The serum glucose and insulin contents and homeostasis model assessment of insulin resistance (HOMA-IR) value of the CS and CE were significantly decreased compared to those of the HS. The PPAR-γ protein expressions in the soleus muscle (SOM) and extensor digitorum longus muscle (EDL) were significantly higher in the CE than in the HS. In addition, the PPAR-γ protein expression in the SOM of the CS was significantly higher than that in the HS. On the other hand, the GLUT-4 protein expression of the SOM in the CE was significantly higher compared to that in the HS. However, there was no significant difference in GLUT-4 protein expression in the EDL among the groups.
Conclusion:CLA supplementation with/without endurance exercise has role in improvement of insulin sensitivity. Moreover, when CLA supplementation was accompanied by endurance exercise, the PPAR-γ protein expression in SOM and EDL and the GLUT-4 protein expression in SOM were enhanced compared with the control group.
https://ijbms.mums.ac.ir/article_6410_bd8e4b0401a56b04adcabd076b789028.pdf
2016-01-01
20
27
10.22038/ijbms.2016.6410
Conjugated linoleic acid
Endurance exercise Insulin
PPAR-γ
GLUT-4
Kangok
Cho
okcho1@snu.ac.kr
1
Institute of Sports Health Science, Sunmoon University, Asan city, Chung Nam, 380-701, S. Korea
AUTHOR
Youngju
Song
song6711@sunmoon.ac.kr
2
Institute of Sports Health Science, Sunmoon University, Asan city, Chung Nam, 380-701, S. Korea
AUTHOR
Daekeun
Kwon
ksunsu@hanmail.net
3
Institute of Sports Health Science, Sunmoon University, Asan city, Chung Nam, 380-701, S. Korea
LEAD_AUTHOR
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26.Park Y, Albright KJ, Liu W, Storkson JM, Cook ME, Pariza MW. Effect of conjugated linoleic acid on body composition in mice. Lipids 1997; 32:853-858.
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27.Koba K, Akahoshi A, Yamasaki M, Tanaka K, Yanada K, Iwata T, et al. Dietary conjugated linoleic acid in relation to CLA differently modifies body fat mass and serum and liver lipid levels in rats. Lipids 2002; 37:343-350.
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28.Poulos SO, Sisk M, Hausman DB, Azain MJ, Hausman GJ. Pre- and postnatal dietary conjugated linoleic acid alters adipose development, body weight gain and body composition in Sprague-Dawley rats. J Nutr 2001; 131:2722-2731.
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29.Kim CH, Youn JH, Park JY, Hong SK, Park KS, Park SW, et al. Effects of high-fat diet and exercise training on intracellular glucose metabolism in rats. Am J Physiol Endocrinol Metab 2000; 278:977-984.
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30.Costa-Júnior JM, Ferreira SM, Protzek AO, Santos GJ, Cappelli AP, Silveira LR, et al. Endurance training inhibits insulin clearance and IDE expression in Swiss mice. PLoS One 2015; 10:e0118809.
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31.Yamasaki B, Ikeda A, Oji M, Tanaka Y, Hirao A, Kasai M, et al. Modulation of body fat and serum leptin levels by dietary conjugated linoleic acid in Sprague Dawley rats fad various fat-level diets. Nutrition 2003; 19:30-35.
31
32.Hariri N, Thibault L. High-fat diet induced obesity in animal models. Nutr Res Rev 2010; 23:270-299.
32
33.Eu CH, Lim WY, Ton SH, bin Abdul Kadir K. Glycyrrhizic acid improved lipoprotein lipase expression, insulin sensitivity, serum lipid and lipid deposition in high-fat diet induced obese rats. Lipids Health Dis 2010; 9:81-89.
33
34.Straczkowski M, Kowaiska I, Dzienis-Straczkowska S, Kinalski M, Górski J, Kinalska L. The effect of exercise training on glucose tolerance and skeletal muscle triacylglycerol content in rats fed with a high-fat diet. Diabetes Metab 2001; 27:19-23.
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35.Haghshenas R, Jafari M, Ravasi A, Kordi M, Gilani N, Shariatzadeh M, et al. The effect pf eight weeks endurance training and high-fat diet on appetite-regulating hormones in rat plasma. Iran J Basic Med Sci 2014; 17:237-243.
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36.Tarnopolosky M, Zimmer A, Paikin J, Safdar A, Aboud A, Pearce E, et al. Creatine monohydrate and conjugated linoleic acid improve strength and body composition following resistance exercise in older adults. PLoS One 2007; 2:e99120.
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37.Patureau Mirand P, Mosoni L, Arnal-Bagnard MA, Faulconnier Y, Chardigny JM, Chilliard Y. Dietary conjugated linoleic acid has limited effects on tissue protein anabolism in sedentary and exercising adult rats. Reprod Nutr Dev 2006; 46:621-632.
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38.Livisay SA, Zhou S, Ip C, Decker EA. Impact of dietary conjugated linoleic acid on the oxidative stability of rat liver microsomes and skeletal muscle homogenates. J Agric Food Chem 2000; 48:4162-4167.
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42.Vyas D, Kadegowda AKG, Erdman RA. Dietary conjugated linoleic acid hepatic steatosis: Species-specific effects on liver and adipose lipid metabolism and gene expression. J Nutr Metab 2012; 2012:932928-932940.
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45.Kumar PM, Venkataranganna MV, Manjunath K, Viswanatha GL, Ashok G. Methanolic extract of Momordica cymbalaria enhances glucose uptake in L6 myotubes in vitro by up-regulating PPAR-γ and GLUT-4. Chin J Nat Med 2014; 12:895-900.
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46.Li M, Bai Y, Chen C, Cui J, Xu X, Dai Y. Effects of exercise and conjugated linoleic acid on PPARγ in adolescent obese rats. Wei Sheng Yan Jiu 2015; 44:179-184.
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47.Li M, Bai Y, Jianfei C, Xiaodong X, Yuanyuan D, Jing Z. Effects of different exercise intensity on PPARγ and relative index in adolescent obesity rats. Wei Sheng Yan Jiu 2014; 43:732-737.
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48.Phillippe PM, Laurent M, Marie-Agnes AB, Yannick F, Jean-Michel C, Yves C. Dietary conjugated linoleic acid has limited effects on tissue protein anabolism in sedentary and exercising adult rats. Reprod Nutr Dev 2006; 46:621-632.
48
49.Lira FS, Yamahita AS, Uchida MC, Zanchi NE, Guaiano B, Martins JE, et al. Low and moderate rather than high intensity strength exercise induces benefit regarding plasma lipid profile. Diabetol Metab Syndr 2010; 2:31-36.
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52.Kolka CM, Richey JM, Castro AV, Broussard JL, Ionut V, Bergman RN. Lipid-induced insulin resistance does not impair insulin access to skeletal muscle. Am J Physiol Endocrinol Metab 2015; [Epub ahead of print].
52
ORIGINAL_ARTICLE
Inactivation of mitogen-activated protein kinase signaling pathway reduces caspase-14 expression in impaired keratinocytes
Objective(s):Several investigations have revealed that caspase-14 is responsible for the epidermal differentiation and cornification, as well as the regulation of moisturizing effect. However, the precise regulation mechanism is still not clear. This study was aimed to investigate the expression of caspase-14 in filaggrin-deficient normal human epidermal keratinocytes (NHEKs) and to explore the possible mechanism that contributes to the regulation of caspase-14. Materials and Methods:The filaggrin-deficient NHEKs were induced by transfection with lentivirus (LV) vector encoding small hairpin RNAs (shRNA). The inhibitors SB203580, PD98059 and SP600125 were used for suppressing the expression of p38 mitogen-activated protein kinase (MAPK), p44/42 MAPK and stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK). The expression of filaggrin, p38 MAPK, p44/42 MAPK and SAPK/JNK, caspase-14, keratin1and keratin2 were detected by western blot. Results:In filaggrin-deficient NHEKs, the expression of p38, p44/42 MAPK and SAPK/JNK and caspase-14 were significantly decreased. The inhibition of p38 and SAPK/JNK reduced the expression of caspase-14, while the p44/42 MAPK showed no consistent effects. Moreover, the filaggrin knockdown decreased the expression of keratin2, but had no effects on the level of keratin1. Conclusion: The decreased expression of caspase-14 in filaggrin-deficient NHEKs may be induced by the inactivation of MAPK signaling pathway. These provide a novel perspective to understand the mechanism for the protective effects of filaggrin and caspase-14 on skin barrier function.
https://ijbms.mums.ac.ir/article_6411_b409eb9e7086c3724b66c2cb8c669cb6.pdf
2016-01-01
28
33
10.22038/ijbms.2016.6411
Caspase-14
Filaggrin
MAPK signaling pathway Skin barrier
Ningning
Dang
15318816250@163.com
1
Department of Dermatology, Jinan Central Hospital affiliated to Shandong University, Jinan, Shandong Province, 250013, China
AUTHOR
Shuguang
Pang
2
Department of Endocrinology, Jinan Central Hospital affiliated to Shandong University, Jinan, Shandong Province, 250013, China
AUTHOR
Haiyan
Song
3
Department of Dermatology, Jinan Central Hospital affiliated to Shandong University, Jinan, Shandong Province, 250013, China
AUTHOR
Liguo
An
4
College of Life Science, Shandong Normal University, Jinan Shandong Province, 250014, China
AUTHOR
Xiaoli
Ma
maxl7125@yahoo.com
5
Central Laboratory, Jinan Central Hospital affiliated to Shandong University, Jinan, Shandong Province, 250013, China
LEAD_AUTHOR
1. Madison KC. Barrier function of the skin:“la raison d'etre” of the epidermis. J Investig Dermatol 2003; 121:231-241.
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2. Oji V, Traupe H. Ichthyoses: differential diagnosis and molecular genetics. Eur J Dermatol 2006; 16:349-359.
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3. Akdis CA, Akdis M, Bieber T, Bindslev-Jensen C, Boguniewicz M, Eigenmann P, et al. Diagnosis and treatment of atopic dermatitis in children and adults: European Academy of Allergology and Clinical Immunology/American Academy of Allergy, Asthma and Immunology/PRACTALL Consensus Report. Allergy 2006; 61:969-987.
3
4. Griffiths CE, Barker JN. Pathogenesis and clinical features of psoriasis. Lancet 2007; 370: 263-271.
4
5. Mildner M, Jin J, Eckhart L, Kezic S, Gruber F, Barresi C, et al. Knockdown of filaggrin impairs diffusion barrier function and increases UV sensitivity in a human skin model. J Invest Dermatol 2010; 130:2286-2294.
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6. Eckhart L, Ban J, Fischer H, Tschachler E. Caspase-14: analysis of gene structure and mRNA expression during keratinocyte differentiation. Biochem Biophys Res Commun 2000; 277:655-659.
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7. Eckhart L, Declercq W, Ban J, Rendl M, Lengauer B, Mayer C, et al. Terminal differentiation of human keratinocytes and stratum corneum formation is associated with caspase-14 activation. J Investig Dermatol 2000; 115:1148-1151.
7
8. Lippens S, Kockx M, Knaapen M, Mortier L, Polakowska R, Verheyen A, et al. Epidermal differentiation does not involve the pro-apoptotic executioner caspases, but is associated with caspase-14 induction and processing. Cell Death Differ 2000; 7:1218-1224.
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9. Denecker G, Ovaere P, Vandenabeele P, Declercq W. Caspase-14 reveals its secrets. J Cell Biol 2008; 180:451-458.
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10. Hoste E, Kemperman P, Devos M, Denecker G, Kezic S, Yau N, et al. Caspase-14 is required for filaggrin degradation to natural moisturizing factors in the skin. J Investig Dermatol 2011; 131:2233-2241.
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11. Hsu S, Dickinson D, Borke J, Walsh DS, Wood J, Qin H, et al. Green tea polyphenol induces caspase 14 in epidermal keratinocytes via MAPK pathways and reduces psoriasiform lesions in the flaky skin mouse model. Exp Dermatol 2007; 16:678-684.
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12. Dang N, Pang S, Song H, Bian H, Zhang X, An L, et al. Knockdown of filaggrin influences the epidermal terminal differentiation via MAPK pathway in normal human epidermal keratinocytes. Mol Biol Rep 2014; 6:6.
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13. Palmer CN, Irvine AD, Terron-Kwiatkowski A, Zhao Y, Liao H, Lee SP, et al. Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis. Nat Genet 2006; 38:441-446.
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14. Kezic S, O’Regan GM, Lutter R, Jakasa I, Koster ES, Saunders S, et al. Filaggrin loss-of-function mutations are associated with enhanced expression of IL-1 cytokines in the stratum corneum of patients with atopic dermatitis and in a murine model of filaggrin deficiency. J Allergy Clin Immunol 2012; 129:1031-1039. e1031.
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15. Levin J, Friedlander SF, Del Rosso JQ. Atopic dermatitis and the stratum corneum: part 1: the role of filaggrin in the stratum corneum barrier and atopic skin. J Clin Aesthet Dermatol 2013; 6:16-22.
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16. Handa S. Filaggrin mutations and the skin. Indian J Dermatol Venereol Leprol 2012; 78: 545.
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17. Dang N, Pang S, Song H, An L, Ma X. Filaggrin silencing by shRNA directly impairs the skin barrier function of normal human epidermal keratinocytes and then induces an immune response. Braz J Med Biol Res 2015; 48:39-45.
17
18. Eckert R, Efimova T, Dashti SR, Balasubramanian S, Deucher A, Crish JF, et al. Keratinocyte survival, differentiation, and death: many roads lead to mitogen-activated protein kinase. J Investig Derma-tol Symp Proc 2002; 7:36-40.
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19. Denecker G, Hoste E, Gilbert B, Hochepied T, Ovaere P, Lippens S, et al. Caspase-14 protects against epidermal UVB photodamage and water loss. Nat Cell Biol 2007; 9:666-674.
19
20. Rendl M, Ban J, Mrass P, Mayer C, Lengauer B, Eckhart L, et al. Caspase-14 expression by epidermal keratinocytes is regulated by retinoids in a differentiation-associated manner. J Invest Dermatol 2002; 119:1150-1155.
20
21. Bayo P, Sanchis A, Bravo A, Cascallana JL, Buder K, Tuckermann J, et al. Glucocorticoid receptor is required for skin barrier competence. Endocrinology 2008; 149:1377-1388.
21
22. Lippens S, Kockx M, Denecker G, Knaapen M, Verheyen A, Christiaen R, et al. Vitamin D3 induces caspase-14 expression in psoriatic lesions and enhances caspase-14 processing in organotypic skin cultures. Am J Pathol 2004; 165:833-841.
22
23. Hsu S, Yamamoto T, Borke J, Walsh DS, Singh B, Rao S, et al. Green tea polyphenol-induced epidermal keratinocyte differentiation is associated with coordinated expression of p57/KIP2 and caspase 14. J Pharmacol Exp Ther 2005; 312: 884-890.
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24. McGrath JA, Uitto J. The filaggrin story: novel insights into skin-barrier function and disease. Trends Mol Med 2008; 14:20-27.
24
25. Popp T, Egea V, Kehe K, Steinritz D, Schmidt A, Jochum M, et al. Sulfur mustard induces differentiation in human primary keratinocytes: opposite roles of p38 and ERK1/2 MAPK. Toxicol Lett 2011; 204:43-51.
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26. Efimova T, Broome AM, Eckert RL. A regulatory role for p38 delta MAPK in keratinocyte differentiation. Evidence for p38 delta-ERK1/2 complex formation. J Biol Chem 2003; 278:34277-34285.
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27. Jonak C, Mildner M, Klosner G, Paulitschke V, Kunstfeld R, Pehamberger H, et al. The hsp27kD heat shock protein and p38-MAPK signaling are required for regular epidermal differentiation. J Dermatol Sci 2011; 61:32-37.
27
28. Gazel A, Banno T, Walsh R, Blumenberg M. Inhibition of JNK promotes differentiation of epidermal keratinocytes. J Biol Chem 2006; 281:20530-20541.
28
29. Sandilands A, Sutherland C, Irvine AD, McLean WI. Filaggrin in the frontline: role in skin barrier function and disease. J Cell Sci 2009; 122:1285-1294.
29
ORIGINAL_ARTICLE
Laminin matrix promotes hepatogenic terminal differentiation of human bone marrow mesenchymal stem cells
Objective(s):The application of stem cells holds great promises in cell transplants. Considering the lack of optimal in vitro model for hepatogenic differentiation, this study was designed to examine the effects of laminin matrix on the improvement of in vitro differentiation of human bone marrow mesenchymal stem cells (hBM-MSC) into the more functional hepatocyte-like cells.
Materials and Methods:Characterization of the hBM-MSCs was performed by immunophenotyping and their differentiation into the mesenchymal-derived lineage. Then, cells were seeded on the laminin-coated or tissue culture polystyrene (TCPS). The differentiation was carried out during two steps. Afterward, the expression of hepatocyte markers such as AFP, ALB, CK-18, and CK-19 as well as the expression of C-MET, the secretion of urea, and the activity of CYP3A4 enzyme were determined. Moreover, the cytoplasmic glycogen storage was examined by periodic acid–Schiff (PAS) staining.
Results:The results demonstrated that the culture of hBM-MSC on laminin considerably improved hepatogenic differentiation compared to TCP group. A significant elevated level of urea biosynthesis and CYP3A4 enzyme activity was observed in the media of the laminin-coated differentiated cells (P<0.05). Furthermore higher expressions of both AFP and ALB were determined in cells differentiated on laminin matrix. Glycogen accumulation was not detected in the undifferentiated hBM-MSCs, however, both differentiated cells in laminin and TCPS groups demonstrated the intracellular glycogen accumulation on day 21 of hepatogenic differentiation.
Conclusion:Taken together, these findings may indicate that laminin matrix can improve terminal differentiation of hepatocyte-like cells from hBM-MSCs. Thus, laminin might be considered as a suitable coating in hepatic tissue engineering designs.
https://ijbms.mums.ac.ir/article_6412_1a1645fd8d0d8126bd09b31990d9e71e.pdf
2016-01-01
34
42
10.22038/ijbms.2016.6412
bone marrow
Differentiation
Hepatocyte
Laminin
Mesenchymal stem cell
Zahra
Khalaj
1
Animal and Marine Biotechnology Department, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran
AUTHOR
Abbas
Sahebghadam Lotfi
lotfi_ab@modares.ac.ir
2
Animal and Marine Biotechnology Department, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran
LEAD_AUTHOR
Maryam
Kabir-Salmani
3
Biomaterials and Tissue Engineering Department, Stem Cell Division, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran
AUTHOR
1. Li J, Li M, Niu B, Gong J. Therapeutic potential of stem cell in liver regeneration. Front Med 2011; 5:26-32.
1
2.O'Leary JG, Lepe R, Davis GL. Indications for liver transplantation. Gastroenterology 2008; 134:1764-1776.
2
3.Kosmacheva S, Seviaryn I, Goncharova N, Petyovka N, Potapnev M. Hepatogenic potential of human bone marrow and umbilical cord blood mesenchymal stem cells. Bull Exp Biol Med 2011; 151:142-149.
3
4.Gómez‐Lechón MJ, Jover R, Donato T, Ponsoda X, Rodriguez C, Stenzel KG, et al. Long‐term expression of differentiated functions in hepatocytes cultured in three‐dimensional collagen matrix. J Cell Physiol 1998; 177:553-562.
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5.Vestentoft PS. Development and molecular composition of the hepatic progenitor cell niche. Dan Med J 2013; 60:B4640.
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6.Spradling A, Drummond-Barbosa D, Kai T. Stem cells find their niche. Nature 2001; 414:98-104.
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7.Fuchs E, Tumbar T, Guasch G. Socializing with the neighbors: stem cells and their niche. Cell 2004; 116:769-778.
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8.Scadden DT. The stem-cell niche as an entity of action. Nature 2006; 441:1075-1079.
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9.Schaffner F, Poper H. Capillarization of hepatic sinusoids in man. Gastroenterology 1963; 44:239-242.
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10. Hahn E, Wick G, Pencev D, Timpl R. Distribution of basement membrane proteins in normal and fibrotic human liver: collagen type IV, laminin, and fibronectin. Gut 1980; 21:63-71.
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11. He H, Liu X, Peng L, Gao Z, Ye Y, Su Y, et al. Promotion of hepatic differentiation of bone marrow mesenchymal stem cells on decellularized cell-deposited extracellular matrix. Biomed Res Int 2013; 2013.
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12. Terada T, Nakanuma Y. Expression of tenascin, type IV collagen and laminin during human intrahepatic bile duct development and in intrahepatic cholangiocarcinoma. Histopathology 1994; 25:143-150.
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13. Martinez-Hernandez A, Delgado FM, Amenta P. The extracellular matrix in hepatic regeneration. Localization of collagen types I, III, IV, laminin, and fibronectin. Lab Invest 1991; 64:157-166.
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14. Wewer UM, Albrechtsen R. Carcinoma-associated perisinusoidal laminin may signal tumour cell metastasis to the liver. Virchows Arch A Pathol Anat Histopathol 1992; 421:87-93.
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15. Quondamatteo F, Scharif K, Herken R. Changes in laminin immunoreactivity as a marker for the state of liver preservation. Histochem J 1994; 26:827-832.
15
16. Friedman SL, Roll FJ, Boyles J, Bissell DM. Hepatic lipocytes: the principal collagen-producing cells of normal rat liver. Proc Natl Acad Sci USA 1985; 82:8681-8685.
16
17. Knittel T, Janneck T, Muller L, Fellmer P, Ramadori G. Transforming growth factor β1‐regulated gene expression of Ito cells. Hepatology 1996; 24:352-360.
17
18. Nikolova G, Strilic B, Lammert E. The vascular niche and its basement membrane. Trends Cell Biol 2007; 17:19-25.
18
19. Tanentzapf G, Devenport D, Godt D, Brown NH. Integrin-dependent anchoring of a stem-cell niche. Nat Cell Biol 2007; 9:1413-1418.
19
20. Tate MC, Garcı́a AJ, Keselowsky BG, Schumm MA, Archer DR, LaPlaca MC. Specific beta1 integrins mediate adhesion, migration, and differentiation of neural progenitors derived from the embryonic striatum. Mol Cell Neurosci 2004; 27:22-31.
20
21. Hayashi Y, Furue MK, Okamoto T, Ohnuma K, Myoishi Y, Fukuhara Y, et al. Integrins regulate mouse embryonic stem cell self‐renewal. Stem Cells 2007; 25:3005-3015.
21
22. Kazemnejad S, Allameh A, Soleimani M, Gharehbaghian A, Mohammadi Y, Amirizadeh N, et al. Biochemical and molecular characterization of hepatocyte-like cells derived from human bone marrow mesenchymal stem cells on a novel three-dimensional biocompatible nanofibrous scaffold. J Gastroenterol Hepatol 2009; 24:278-287.
22
23. Ayatollahi M, Soleimani M, Tabei SZ, Salmani MK. Hepatogenic differentiation of mesenchymal stem cells induced by insulin like growth factor-I. World J Stem Cells 2011; 3:113-121.
23
24. Kallis YN, Robson AJ, Fallowfield JA, Thomas HC, Alison MR, Wright NA, et al. Remodelling of extracellular matrix is a requirement for the hepatic progenitor cell response. Gut 2011; 60:525-533.
24
25. Takayama K, Nagamoto Y, Mimura N, Tashiro K, Sakurai F, Tachibana M, et al. Long-Term Self-Renewal of Human ES/iPS-Derived Hepatoblast-like Cells on Human Laminin 111-Coated Dishes. Stem Cell Reports 2013; 1:322-335.
25
ORIGINAL_ARTICLE
Application of citrate as a tricarboxylic acid (TCA) cycle intermediate, prevents diabetic-induced heart damages in mice
Objective(s):Higher cellular reactive oxygen species (ROS) levels is important in reducing cellular energy charge (EC) by increasing the levels of key metabolic protein, and nitrosative modifications, and have been shown to damage the cardiac tissue of diabetic mice. However, the relation between energy production and heart function is unclear.
Materials and Methods:Streptozotocin (STZ, 150 mg/kg body weight) was injected intraperitoneally once to mice that had been fasted overnight for induction of diabetes. After diabetic induction, mice received citrate (5 µg/kg) through intraperitoneal injection every other day for 5 weeks. The caspase-3, plasminogen activator inhibitor 1 (PAI1), protein kinase B (PKB), commonly known as AKT and phosphorylated-AKT (p-AKT) proteins were examined to elucidate inflammation and apoptosis in the heart. For histological analysis, heart samples were fixed with 10% formalin and stained with hematoxylin-eosin (HE) and Sirius red to assess pathological changes and fibrosis. The expression levels[AGA1] of marker proteins, tyrosine nitration, activity of ATP synthase and succinyl-CoA:3-ketoacid coenzyme A transferase-1 (SCOT), and EC were measured.
Results:Intraperitoneal injection of citrate significantly reduced caspase-3 and PAI-1 protein levels and increased p-AKT level on the 5th week; EC in the heart was found to be increased as well. Further, the expression level, activity, and tyrosine nitration of ATP synthase and SCOT were not affected after induction of diabetes.
Conclusion: Results indicate that application of citrate, a tricarboxylic acid (TCA) cycle intermediate, might alleviate cardiac dysfunction by reducing cardiac inflammation, apoptosis, and increasing cardiac EC.
https://ijbms.mums.ac.ir/article_6413_43d5122b3c7a1108b74030e4664ec76c.pdf
2016-01-01
43
48
10.22038/ijbms.2016.6413
Citrate
Diabetes
Heart
Nitration
Tricarboxylic acid
Qianqian
Liang
1
Department of Emergency, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou, 450007China
AUTHOR
Baoyu
Wang
baoyuwang12@163.com
2
Department of Emergency, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou, 450007China
AUTHOR
Lingxia
Pang
lingxiapang@163.com
3
Function Experiment Teaching Center, Wenzhou Medical University, Wenzhou, 325305China
AUTHOR
Youpei
Wang
wangyoupei@163.com
4
Function Experiment Teaching Center, Wenzhou Medical University, Wenzhou, 325305China
AUTHOR
Meiqin
Zheng
mqzheng1973@163.com
5
The Affiliated Eye Hospital, Wenzhou Medical University, Wenzhou, 325000China
AUTHOR
Qing
Wang
denniswq@yahoo.com
6
The Affiliated Eye Hospital, Wenzhou Medical University, Wenzhou, 325000China
AUTHOR
Jingbin
Yan
13758483130@163.com
7
Department of Pain management, Wenzhou Hospital of integrated Chinese and Western Medicine, Wenzhou, 325000 China
AUTHOR
Jinzhong
Xu
fengzhongjin@163.com
8
Wenling First People’s Hospital, The Affiliated Hospital of Wenzhou Medical University, Wenling, 317500
LEAD_AUTHOR
1. Bonow RO, Gheorghiade M. The diabetes epidemic: a national and global crisis. Am J Med 2004; 116:2S-10S.
1
2. Francis GS. Diabetic cardiomyopathy: fact or fiction? Heart 2001; 85:247-248.
2
3. Kralik PM, Ye G, Metreveli NS, Shem X, Epstein PN. Cardiomyocyte dysfunction in models of type 1 and type 2 diabetes. Cardiovasc Toxicol 2005; 5:285-292.
3
4. Cai L, Kang YJ. Oxidative stress and diabetic cardiomyopathy: a brief review. Cardiovasc Toxicol 2001; 1:181-193.
4
5. Yildirim O, Buyukbingol Z. Effect of cobalt on the oxidative status in heart and aorta of streptozotocin-induced diabetic rats. Cell Biochem Funct 2003; 21:27-33.
5
6. Pacher P, Szabó C. Role of peroxynitrite in the pathogenesis of cardiovascular complications of diabetes. Curr Opin Pharmacol 2006; 6:136-141.
6
7. Giacco F, Brownlee M. Oxidative stress and diabetic complications. Circ Res 2010; 107:1058-1070.
7
8. Marra G, Cotroneo P, Pitocco D, Manto A, Di Leo MA, Ruotolo V, et al. Early increase of oxidative stress and reduced antioxidant defenses in Patients with uncomplicated type 1 diabetes a case for gender difference. Diabetes Care 2002; 25: 370-375.
8
9. Penckofer S, Schwertz D, Florczak K. Oxidative stress and cardiovascular disease in type 2 diabetes: the role of antioxidants and pro-oxidants. J Cardiovasc Nurs 2002; 16: 68-85.
9
10. Shen X, Zheng S, Metreveli NS, Epstein PN. Protection of cardiac mitochondria by overexpression of MnSOD reduces diabetic cardiomyopathy. Diabetes 2006; 55: 798-805.
10
11. Cong W, Zhao T, Zhu Z, Huang B, Ma W, Wang Y, et al. Metallothionein prevents cardiac pathological changes in diabetes by modulating nitration and inactivation of cardiac ATP synthase. J Nutr Biochem 2014; 25:463-474.
11
12. Cong W, Ma W, Zhao T, Zhu Z, Wang Y, Tan Y, et al. Metallothionein prevents diabetes-induced cardiac pathological changes, likely via the inhibition of succinyl-CoA:3-ketoacid coenzyme A transferase-1 nitration at Trp (374). Am J Physiol Endocrinol Metab 2013; 304:E826-E835.
12
13. Lowenstein JM. Methods in Enzymology. Citric Acid Cycle. Boston: Academic Press; 1969.Vol 13.
13
14. Krebs HA, Weitzman PDJ. Krebs' citric acid cycle: half a century and still turning. London: Biochem Soc; 1987.
14
15. Cai L, Wang J, Li Y, Sun X, Wang L, Zhou Z, et al. Inhibition of superoxide generation and associated nitrosative damage is involved in metallothionein prevention of diabetic cardiomyopathy. Diabetes 2005; 54:1829-1837.
15
16. Cai L, Wang Y, Zhou G, Chen T, Song Y, Li X, et al. Attenuation by metallothionein of early cardiac cell death via suppression of mitochondrial oxidative stress results in a prevention of diabetic cardiomyopathy. J Am Coll Cardiol 2006; 48: 1688-1697.
16
17. Wang Y, Peng F, Tong W, Sun H, Xu N, Liu S. The nitrated proteome in heart mitochondria of the db/db mouse model: characterization of nitrated tyrosine residues in SCOT. J Proteome Res2010;9:4254–4263.
17
18. Manfredi G, Yang L, Gajewski CD, Mattiazzi M. Measurements of ATP in mammalian cells. Methods 2002; 26:317-326.
18
19. Zur Nedden S, Hawley S, Pentland N, Hardie DG, Doney AS, Frenguelli BG. Intracellular ATP influences synaptic plasticity in area CA1 of rat hippocampus via metabolism to adenosine and activity-dependent activation of adenosine A1 receptors. J Neurosci 2011; 31:6221-6234.
19
20. Atkinson DE. The energy charge of the adenylate pool as a regulatory parameter. Interaction with feedback modifiers. Biochemistry 1968; 7:4030-4034.
20
21. Zhao J, Zhang H, Huang Y, Wang H, Wang S, Zhao C, et al. Bay11-7082 attenuates murine lupus nephritis via inhibiting NLRP3 inflammasome and NF-kappaB activation. Int Immunopharmacol 2013; 17:116-122.
21
22. Aulak KS, Miyagi M, Yan L, West KA, Massillon D, Crabb JW, et al. Proteomic method identifies proteins nitrated in vivo during inflammatory challenge.Proc Natl Acad Sci USA 2001; 98:12056-12061.
22
ORIGINAL_ARTICLE
The effect of adrenomedullin and proadrenomedullin N- terminal 20 peptide on angiotensin II induced vascular smooth muscle cell proliferation
Objective(s): The study aimed to investigate the effects of adrenomedullin (ADM) and proadrenomedullin N- terminal 20 peptide (PAMP) on angiotensin II (AngII)-stimulated proliferation in vascular smooth muscle cells (VSMCs).
Materials and Methods: Thoracic aorta was obtained from Wistar rats and VSMCs were isolated from aorta tissues and then cultured. In vitro cultured VSMCs were stimulated with Ang II (10-8 mol/l) followed by various doses of PAMP or ADM (10-9, 10-8, or 10-7 mol/l). Cell proliferation as assessed by 3H-TdR incorporation. Protein kinase C (PKC) activity was measured by counting γ-32P radioactivity with liquid scintillation. In a separate cohort, in vitro cultured rat aortic vessels were treated with different doses of Ang II or PAMP (10-9, 10-8, or 10-7 mol/l). Cellular and secreted levels of PAMP, ADM and Ang II were measured using radioimmunoassay in the tissues and intubation mediums, respectively.
Results: Ang II (10-8 mol/l) treatment significantly increased both 3H-TdR incorporation and PKC activity in VSMCs (by 2.68 and 1.02-fold, respectively; both P<0.01 vs. the control). However, Ang II-induced elevation of 3H-TdR incorporation, and PKC activity was significantly inhibited by various doses of ADM and PAMP (all P<0.01 vs. the Ang II group). In rat aortic vascular tissues or intubation media, Ang II treatments stimulated the expression and secretion of PAMP and ADM in a dose-dependent manner, while PAMP treatments had no significant effects on Ang II levels.
Conclusion: ADM and PAMP inhibit Ang II-induced VSMCs proliferation. The interaction of Ang II, ADM and PAMP may regulate VSMCs and cardiovascular function.
https://ijbms.mums.ac.ir/article_6414_1b5275a739e8ef4f1e84488c221c9d6b.pdf
2016-01-01
49
54
10.22038/ijbms.2016.6414
Adrenomedulin
Angiotension II
Proadrenomedullin N-terminal 20 peptide
Proliferation
Vascular smooth muscle- cell
Jian
Ma
majian4780@163.com
1
Cadres Division One, The 401st Hospital of PLA, Qingdao 266071, China
LEAD_AUTHOR
Yinglu
Feng
ylfeng1975@yahoo.com.cn
2
Cadres Division One, The 401st Hospital of PLA, Qingdao 266071, China
AUTHOR
Zaiquan
Li
lizaiquan@bjmu.edu.cn
3
Institute of Cardiovascular Research, Peking Medical University, First Hospital, Beijing 100083, China
AUTHOR
Chaoshu
Tang
tangchaoshu@263.net.cn
4
Institute of Cardiovascular Research, Peking Medical University, First Hospital, Beijing 100083, China
AUTHOR
1. Nishikimi T, Kuwahara K, Nakagawa Y, Kangawa K, Nakao K. Adrenomedullin in cardiovascular diseases: a useful biomarker, its pathological roles and therapeutic application. Curr Protein Pept Sci 2013; 14:256-67.
1
2. Hirata Y, Takagi Y, Takata S, Fukuda Y, Yoshimi H, Fujita T. Calcitonin gene-related peptide receptor in cultured vascular smooth muscle and endothelial cells. Biochem Biophys Res Commun 1988; 151:1113-1121.
2
3. Haller H, Baur E, Quass P, Behrend M, Lindschau C, Distler A, et al. High glucose concentrations and protein kinase C isoforms in vascular smooth muscle cells. Kidney Int 1995; 47:1057-1067.
3
4. Shimosawa T, Fujita T. Hypotensive effect of a newly identified peptide, proadrenomedullin N-terminal 20 peptide. Hypertension 1996; 28:325-329.
4
5. Sugo S, Minamino N, Kangawa K, Miyamoto K, Kitamura K, Sakata J, et al. Endothelial cells actively synthesize and secrete adrenomedullin. Biochem Biophys Res Commun 1994; 201:1160-1166.
5
6. Eto T. A review of the biological properties and clinical implications of adrenomedullin and proadrenomedullin N-terminal 20 peptide (PAMP), hypotensive and vasodilating peptides. Peptides 2001; 22:1693-711.
6
7. Shimekake Y, Nagata K, Ohta S, Kambayashi Y, Teraoka H, Kitamura K, et al. Adrenomedullin stimulates two signal transduction pathways, cAMP accumulation and Ca2+ mobilization, in bovine aortic endothelial cells. J Biol Chem 1995; 270:4412-4417.
7
8. Takano K, Yamashita N, Fujita T. Proadrenomedu-llin NH2-terminal 20 peptide inhibits the voltage-gated Ca2+ channel current through a pertussis toxin-sensitive G protein in rat pheochromocytoma-derived PC 12 cells. J Clin Invest 1996; 98:14-17.
8
9. Inatsu H, Sakata J, Shimokubo T, Kitani M, Nishizono M, Washimine H, et al. Distribution and characterization of rat immunoreactive proadreno-medullin N-terminal 20 peptide (PAMP) and the augmented cardiac PAMP in spontaneously hypertensive rat. Biochem Mol Biol Int 1996; 38:365-372.
9
10. Sims C, Ashby K, Douglas JG. Angiotensin II-induced changes in guanine nucleotide binding and regulatory proteins. Hypertension 1992; 19:146-152.
10
11. Andreis PG, Markowska A, Champion HC, Mazzocchi G, Malendowicz LK, Nussdorfer GG. Adrenomedullin enhances cell proliferation and deoxyribonucleic acid synthesis in rat adrenal zona glomerulosa: receptor subtype involved and signaling mechanism. Endocrinology 2000; 141:2098-2104.
11
12. Goichberg P, Kalinkovich A, Borodovsky N, Tesio M, Petit I, Nagler A, et al. cAMP-induced PKCzeta activation increases functional CXCR4 expression on human CD34+ hematopoietic progenitors. Blood 2006; 107:870-879.
12
13. Hinson JP, Kapas S, Smith DM. Adrenomedullin, a multifunctional regulatory peptide. Endocr Rev 2000; 21:138-167.
13
14. Rossi F, Bertone C, Petricca S, Santiemma V. Adrenomedullin antagonizes angiotensin II-stimulated proliferation of human aortic smooth muscle cells. Peptides 2006; 27:2935-41.
14
15. Hamid SA, Baxter GF. Adrenomedullin: regulator of systemic and cardiac homeostasis in acute myocardial infarction. Pharmacol Ther 2005; 105:95-112.
15
ORIGINAL_ARTICLE
Effect of bone marrow derived mesenchymal stem cells on lung pathology and inflammation in ovalbumin-induced asthma in mouse
Objective(s):Bone marrow-derived mesenchymal stem cells (BMSCs) have attracted significant interest to treat asthma and its complication. In this study, the effects of BMSCs on lung pathology and inflammation in an ovalbumin-induced asthma model in mouse were examined. Materials and Methods:BALB/c mice were divided into three groups: control group (animals were not sensitized), asthma group (animals were sensitized by ovalbumin), asthma+BMSC group (animals were sensitized by ovalbumin and treated with BMSCs). BMSCs were isolated and characterized and then labeled with Bromodeoxyuridine (BrdU). After that the cells transferred into asthmatic mice. Histopathological changes of the airways, BMSCs migration and total and differential white blood cell (WBC) count in bronchoalveolar lavage (BAL) fluid were evaluated. Results:A large number of BrdU-BMSCs were found in the lungs of mice treated with BMSCs. The histopathological changes, BAL total WBC counts and the percentage of neutrophils and eosinophils were increased in asthma group compared to the control group. Treatment with BMSCs significantly decreased airway pathological indices, inflammatory cell infiltration, and also goblet cell hyperplasia. Conclusion:The results of this study revealed that BMSCs therapy significantly suppressed the lung pathology and inflammation in the ovalbumin induced asthma model in mouse.
https://ijbms.mums.ac.ir/article_6415_5fdd7524b52de812fd3eacafcd585273.pdf
2016-01-01
55
63
10.22038/ijbms.2016.6415
Inflammation
Lung pathology
Ovalbumin- induced asthma
Stem cells
Maryam
Mohammadian
maryam.mohammadian2008@yahoo.com
1
Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Mohammad Hosein
Boskabady
2
Neurogenic Inflammation Research Center and Department of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Iraj
Ragerdi Kashani
ragerdi@sina.tums.ac.ir
3
Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Gila Pirzad
Jahromi
4
Neuroscience Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran
AUTHOR
Amene
Omidi
omidi_amene@yahoo.com
5
Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Amir
Kavian Nejad
amirkaviannejad@yahoo.com
6
Department of Emergency Medical Services, School of Nursing and Midwifery, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Safoura
Khamse
s.khamseh90@yahoo.com
7
Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Hamid Reza
Sadeghipour
sadeghipour@tums.ac.ir
8
Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
1.Nakagome K, Nagata M. Pathogenesis of airway inflammation in bronchial asthma. Auris Nasus Larynx 2011; 38:555-563.
1
2.Bloemen K, Verstraelen S, Van Den Heuvel R, Witters H, Nelissen I, Schoeters G. The allergic cascade: review of the most important molecules in the asthmatic lung. Immunol Lett 2007; 113:6-18.
2
3.Al-Muhsen S, Johnson JR, Hamid Q. Remodeling in asthma. J Allergy Clin Immunol 2011; 128:451-462.
3
4.Bergeron C, Tulic MK, Hamid Q. Airway remodelling in asthma: from benchside to clinical practice. Can Respir J 2010; 17:85-93.
4
5.Girodet PO, Ozier A, Bara I, Tunon de Lara JM, Marthan R, Berger P. Airway remodeling in asthma: new mechanisms and potential for pharmacological intervention. Pharmacol Ther 2011; 130:325-337.
5
6.Cavkaytar O, Vuralli D, Arik Yilmaz E, Buyuktiryaki B, Soyer O, Sahiner UM, et al. Evidence of hypothalamic-pituitary-adrenal axis suppression during moderate-to-high-dose inhaled corticosteroid use. Eur J Pediatr 2015; 174:1421-1431.
6
7.Baker N, Boyette LB, Tuan RS. Characterization of bone marrow-derived mesenchymal stem cells in aging. Bone 2015;70:37-47.
7
8.Bonfield TL, Caplan AI. Adult mesenchymal stem cells: an innovative therapeutic for lung diseases. Discov Med 2010; 9:337-345.
8
9.Tessier L, Bienzle D, Williams LB, Koch TG. Phenotypic and immunomodulatory properties of equine cord blood-derived mesenchymal stromal cells. PLoS One 2015;10:e0122954.
9
10. Mohammadian M, Abasi E, Akbarzadeh A. Mesenchymal stem cell-based gene therapy: A promising therapeutic strategy. Artif Cells Nanomed Biotechnol. 2015:1-6. [Epub ahead of print]
10
11. Rabani V, Shahsavani M, Gharavi M, Piryaei A, Azhdari Z, Baharvand H. Mesenchymal stem cell infusion therapy in a carbon tetrachloride-induced liver fibrosis model affects matrix metalloproteinase expression. Cell Biol Int 2010; 34:601-605.
11
12. Moodley Y, Atienza D, Manuelpillai U, Samuel CS, Tchongue J, Ilancheran S, et al. Human umbilical cord mesenchymal stem cells reduce fibrosis of bleomycin-induced lung injury. Am J Pathol 2009; 175:303-313.
12
13. Lee SH, Jang AS, Kim YE, Cha JY, Kim TH, Jung S, et al. Modulation of cytokine and nitric oxide by mesenchymal stem cell transfer in lung injury/fibrosis. Respir Res 2010; 11:16.
13
14.Semedo P, Correa-Costa M, Antonio Cenedeze M, Maria Avancini Costa Malheiros D, Antonia dos Reis M, Shimizu MH, et al. Mesenchymal stem cells attenuate renal fibrosis through immune modulation and remodeling properties in a rat remnant kidney model. Stem cells 2009; 27:3063-3073.
14
15. Deng W, Chen QW, Li XS, Liu H, Niu SQ, Zhou Y, et al. Bone marrow mesenchymal stromal cells with support of bispecific antibody and ultrasound-mediated microbubbles prevent myocardial fibrosis via the signal transducer and activators of transcription signaling pathway. Cytotherapy 2011; 13:431-440.
15
16. Molina EJ, Palma J, Gupta D, Torres D, Gaughan JP, Houser S, et al. Reverse remodeling is associated with changes in extracellular matrix proteases and tissue inhibitors after mesenchymal stem cell (MSC) treatment of pressure overload hypertrophy. J Tissue Eng Regen Med 2009; 3:85-91.
16
17.Firinci F, Karaman M, Baran Y, Bagriyanik A, Ayyildiz ZA, Kiray M, et al. Mesenchymal stem cells ameliorate the histopathological changes in a murine model of chronic asthma. Int Immunopharmacol 2011; 11:1120-1126.
17
18.Ogulur I, Gurhan G, Kombak FE, Filinte D, Barlan I, Akkoc T. Allogeneic pluripotent stem cells suppress airway inflammation in murine model of acute asthma. Int Immunopharmacol 2014; 22:31-40.
18
19.Cho KS, Park MK, Kang SA, Park HY, Hong SL, Park HK, et al. Adipose-derived stem cells ameliorate allergic airway inflammation by inducing regulatory T cells in a mouse model of asthma. Mediators Inflamm 2014; 2014:436-476.
19
20.Ogulur I, Gurhan G, Aksoy A, Duruksu G, Inci C, Filinte D, et al. Suppressive effect of compact bone-derived mesenchymal stem cells on chronic airway remodeling in murine model of asthma. Int Immunopharmacol 2014; 20:101-109.
20
21.Pirzad Jahromi G, Seidi S, Sadr SS, Shabanzadeh AP, Keshavarz M, Kaka GR, et al. Therapeutic effects of a combinatorial treatment of simvastatin and bone marrow stromal cells on experimental embolic stroke. Basic Clin Pharmacol Toxicol 2012; 110:487-493.
21
22.Kashani IR, Golipoor Z, Akbari M, Mahmoudi R, Azari S, Shirazi R, et al. Schwann-like cell differentiation from rat bone marrow stem cells. Arch Med Sci 2011; 7:45-52.
22
23.Song X, Xie S, Lu K, Wang C. Mesenchymal stem cells alleviate experimental asthma by inducing polarization of alveolar macrophages. Inflammation 2015; 38:485-492.
23
24.Zaminy A, Kashani IR, Barbarestani M, Hedayatpour A, Mahmoudi R, Farzaneh Nejad AR. Osteogenic Differentiation of Rat Mesenchymal Stem Cells from Adipose Tissue in Comparison with Bone Marrow Mesenchymal Stem Cells: Melatonin As a Differentiation Factor. Iran Biomed J 2008; 12:133-141.
24
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26.Qian C, Tio RA, Roks AJ, Boddeus KM, Harmsen MC, van Gilst WH, et al. A promising technique for transplantation of bone marrow-derived endothelial progenitor cells into rat heart. Cardiovasc Pathol 2007; 16:127-135.
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27.Khakzad MR, Mirsadraee M, Mohammadpour A, Ghafarzadegan K, Hadi R, Saghari M, et al. Effect of verapamil on bronchial goblet cells of asthma: an experimental study on sensitized animals. Pulm Pharmacol Ther 2012; 25:163-168.
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28.Cao R, Dong XW, Jiang JX, Yan XF, He JS, Deng YM, et al. M(3) muscarinic receptor antagonist bencycloquidium bromide attenuates allergic airway inflammation, hyperresponsiveness and remodeling in mice. Eur J Pharmacol 2011; 655:83-90.
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32.Wang Y, Deng Y, Zhou GQ. SDF-1alpha/CXCR4-mediated migration of systemically transplanted bone marrow stromal cells towards ischemic brain lesion in a rat model. Brain Res 2008; 1195:104-112.
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34.Yu J, Li M, Qu Z, Yan D, Li D, Ruan Q. SDF-1/CXCR4-mediated migration of transplanted bone marrow stromal cells toward areas of heart myocardial infarction through activation of PI3K/Akt. J Cardiovasc Pharmacol 2010; 55:496-505.
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35.Ou-Yang HF, Huang Y, Hu XB, Wu CG. Suppression of allergic airway inflammation in a mouse model of asthma by exogenous mesenchymal stem cells. Exp Biol Med (Maywood) 2011; 236:1461-1467.
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37.Neamati A, Boskabady MH, Mohaghegh Hazrati S, Khakzad MR, Moosavi SH. The effect of natural adjuvants (G2, G2F) on lung inflammation of sensitized guinea pigs. Avicenna J Phytomed 2013; 3:364-370.
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38.Bonfield TL, Koloze M, Lennon DP, Zuchowski B, Yang SE, Caplan AI. Human mesenchymal stem cells suppress chronic airway inflammation in the murine ovalbumin asthma model. Am J Physiol Lung Cell Mol Physiol 2010; 299:760-770.
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39.Kapoor S, Patel SA, Kartan S, Axelrod D, Capitle E, Rameshwar P. Tolerance-like mediated suppression by mesenchymal stem cells in patients with dust mite allergy-induced asthma. J Allergy Clin Immunol 2012; 129:1094-1101.
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40.Atsma DE, Fibbe WE, Rabelink TJ. Opportunities and challenges for mesenchymal stem cell-mediated heart repair. Curr Opin Lipidol 2007; 18:645-649.
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41.Le Blanc K, Ringden O. Immunomodulation by mesenchymal stem cells and clinical experience. J Intern Med 2007; 262:509–25.
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42.Abreu SC, Antunes MA, de Castro JC, de Oliveira MV, Bandeira E, Ornellas DS, et al. Bone marrow-derived mononuclear cells vs. mesenchymal stromal cells in experimental allergic asthma. Respir Physiol Neurobiol 2013; 187:190-198.
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43.Ghorbani A, Feizpour A, Hashemzahi M, Gholami L, Hosseini M, Soukhtanloo M, et al. The effect of adipose derived stromal cells on oxidative stress level, lung emphysema and white blood cells of guinea pigs model of chronic obstructive pulmonary disease. Daru J Pharmac Sci 2014; 22:26.
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44.Feizpour A, Ghorbani A, Boskabady MH. Adipose-derived stromal cell therapy affects lung inflammation and tracheal responsiveness in guinea pig model of COPD. PLoS ONE 2014; 9: e108974.
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45.Boskabady MH, Keyhanmanesh R, Khamneh S, Doostar Y. Potential immunomodulation effect of Nigella sativa on ovalbumin sensitized guinea pigs. J Zhejiang Univ Sci B 2011; 12:201-209.
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46. Boskabady MH, Shahmohammadi Mehrjardi S, Rezaee A, Rafatpanah H, jalali S. The impactof Zataria multiflora Boiss extracton in vitro and in vivo Th1/Th2 cytokine (IFN-γ/IL4) balance. J Ethnopharmacpol 2013; 150:1024-1031.
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47.Bayrami G, Boskabady MH, Jalali S, Farkhondeh T. The effect of the extract of Crocus sativus on tracheal responsiveness and plasma levels of IL-4, IFN-γ, total NO and nitrite in ovalbumin sensitized Guinea-pigs. J EthnoPharmacol 2013; 147:530-535.
47
ORIGINAL_ARTICLE
Lung-derived innate cytokines: new epigenetic targets of allergen-specific sublingual immunotherapy
Objective(s):Sublingual allergen-specific immunotherapy is a safe and effective method for treatment of IgE-mediated respiratory allergies; however, the underlying mechanisms are not fully understood. This study was planned to test whether sublingual immunotherapy (SLIT) can exert epigenetic mechanisms through which the airway allergic responses can be extinguished. Materials and Methods:BALB/c mice were sensitized intraperitoneally and challenged intranasally. Then, they received sublingual treatment with recombinant Che a 2 (rChe a 2), a major allergen of Chenopodium album. After SLIT, allergen-specific antibodies in sera, cytokine profiles of spleen cell cultures, mRNA and protein expression of lung-derived IL-33, IL-25, and TSLP (thymic stromal lymphopoietin), and histone modifications of these three genes were assessed. Results:Following Immunotherapy, systemic immune responses shifted from Th2 to Th1 profile as demonstrated by significant decrease in IgE and IL-4 and substantial increase in IgG2a and IFN-γ. At local site, mRNA and protein levels of lung-derived pro-inflammatory cytokines IL-33 and TSLP were markedly down-regulated following SLIT that was associated with marked enrichment of trimethylated lysine 27 of histone H3 at promoter regions of these two cytokines. Conclusion:In our study, sublingual immunotherapy with recombinant allergen effectively attenuated allergic immune responses, at least partly, by induction of distinct histone modifications at specific loci. Additionally, the lung-derived pro-allergic cytokines IL-33 and TSLP could be promising mucosal candidates for either monitoring allergic conditions or therapeutic approaches.
https://ijbms.mums.ac.ir/article_6416_036caed31e21cd3ee172d87e2e7d1b70.pdf
2016-01-01
64
71
10.22038/ijbms.2016.6416
Chenopodium album Histone modifications
IL-25
IL-33
Sublingual mmunotherapy
TSLP
Abbas
Pishdadian
pishdadiana891@mums.ac.ir
1
School of Medicine, Zabol University of Medical Sciences, Zabol, Iran
AUTHOR
Abdolreza
Varasteh
2
Allergy Research Center, Medical School, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mehran
Gholamin
golaminm@mums.ac.ir
3
Division of Human Genetics, Immunology Research Center, Avicenna Research Institute, Mashhad University of Medical Sciences,Mashhad, Iran
AUTHOR
Leila
Roozbeh Nasiraie
leila_roozbeh@yahoo.com
4
Department of Food Science, Nour Branch, Islamic Azad University, Nour, Iran
AUTHOR
Mitra
Hosseinpour
hoseinpourm4@mums.ac.ir
5
Immunology Research Center, Medical School, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Malihe
Moghadam
moghadamm1@mums.ac.ir
6
Immunology Research Center, Medical School, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mojtaba
Sankian
sankianm@mums.ac.ir
7
Immunology Research Center, Medical School, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
1. Canonica GW, Cox L, Pawankar R, Baena-Cagnani CE, Blaiss M, Bonini S, et al. Sublingual immunotherapy: World Allergy Organization position paper 2013 update. World Allergy Organ J 2014; 7:6.
1
2. Swamy RS, Reshamwala N, Hunter T, Vissamsetti S, Santos CB, Baroody FM, et al. Epigenetic modifications and improved regulatory T-cell function in subjects undergoing dual sublingual immunotherapy. J Allergy Clin Immunol 2012; 130:215-224 e7.
2
3. Cheng RY, Shang Y, Limjunyawong N, Dao T, Das S, Rabold R, et al. Alterations of the lung methylome in allergic airway hyper-responsiveness. Environ Mol Mutagen 2014; 55:244-255.
3
4. Brand S, Kesper DA, Teich R, Kilic-Niebergall E, Pinkenburg O, Bothur E, et al. DNA methylation of TH1/TH2 cytokine genes affects sensitization and progress of experimental asthma. J Allergy Clin Immunol 2012; 129:1602-1610 e6.
4
5. Shang Y, Das S, Rabold R, Sham JS, Mitzner W, Tang WY. Epigenetic alterations by DNA methylation in house dust mite-induced airway hyperrespon-siveness. Am J Respir Cell Mol Biol 2013; 49:279-287.
5
6. Harb H, Renz H. Update on epigenetics in allergic disease. J Allergy Clin Immunol 2015; 135:15-24.
6
7. Holtzman MJ, Byers DE, Alexander-Brett J, Wang X. The role of airway epithelial cells and innate immune cells in chronic respiratory disease. Nat Rev Immunol. 2014; 14:686-698.
7
8. Bartemes KR, Kita H. Dynamic role of epithelium-derived cytokines in asthma. Clin Immunol 2012; 143:222-235.
8
9. Barderas R, Villalba M, Pascual CY, Batanero E, Rodriguez R. Profilin (Che a 2) and polcalcin (Che a 3) are relevant allergens of Chenopodium album pollen: isolation, amino acid sequences, and immunologic properties. J Allergy Clin Immunol 2004; 113:1192-1198.
9
10. Villalba M, Barderas R, Mas S, Colas C, Batanero E, Rodriguez R. Amaranthaceae pollens: review of an emerging allergy in the mediterranean area. J Investig Allergol Clin Immunol 2014; 24:371-381.
10
11. Fereidouni M, Hossini RF, Azad FJ, Assarehzadegan MA, Varasteh A. Skin prick test reactivity to common aeroallergens among allergic rhinitis patients in Iran. Allergol Immunopathol (Madr) 2009; 37:73-79.
11
12. Assarehzadegan MA, Shakurnia A, Amini A. The most common aeroallergens in a tropical region in Southwestern Iran. World Allergy Organ J 2013; 6:7.
12
13. Ahmadiafshar A, Sepehri S, Mousavinasab S, Torabi SZ. Recognition and frequency of common allergens in allergic patients of zanjan by skin prick test. Zanjan Univ Med Sci J 2008; 16:45-53.
13
14. Amini A, sankian M, Assarehzadegan MA, Vahedi F, Varasteh A. Chenopodium album pollen profilin (Che a 2): homology modeling and evaluation of cross-reactivity with allergenic profilins based on predicted potential IgE epitopes and IgE reactivity analysis. Mol Biol Rep. 2011; 38:2579-2587. Epub 2010/11/19.
14
15. Nouri HR, Sankian M, Afsharzadeh D, Varasteh A. Immunotherapy with a recombinant hybrid molecule alleviates allergic responses more efficiently than an allergenic cocktail or pollen extract in a model of Chenopodium album allergy. Int Arch Allergy Immunol 2013; 161:325-332.
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16. Pfaffl MW. A new mathematical model for relative quantification in real-time RT–PCR. Nuclic Acids Res 2001; 29:e45.
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17. Smith P, Krohn RI, Hermanson G, Mallia A, Gartner F, Provenzano M, et al. Measurement of protein using bicinchoninic acid. Anal Biochem 1985; 150:76-85.
17
18. Nouri HR, Varasteh A, Vahedi F, Chamani J, Afsharzadeh D, Sankian M. Constructing a hybrid molecule with low capacity of IgE binding from Chenopodium album pollen allergens. Immunol lett 2012; 144:67-77.
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19. Taylor SC, Berkelman T, Yadav G, Hammond M. A defined methodology for reliable quantification of Western blot data. Mol Biotechnol 2013; 55:217-226.
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20. Sailaja BS, Takizawa T, Meshorer E. Chromatin immunoprecipitation in mouse hippocampal cells and tissues. Methods Mol Biol 2012; 809:353-64.
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21. Negishi H, Miki S, Sarashina H, Taguchi-Atarashi N, Nakajima A, Matsuki K, et al. Essential contribution of IRF3 to intestinal homeostasis and microbiota-mediated Tslp gene induction. Proc Natl Acad Sci U S A 2012; 109:21016-21021.
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22. Wang Z, Zhang LJ, Guha G, Li S, Kyrylkova K, Kioussi C, et al. Selective ablation of Ctip2/Bcl11b in epidermal keratinocytes triggers atopic dermatitis-like skin inflammatory responses in adult mice. PLoS One 2012; 7:e51262.
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23. Lefrançais E, Roga S, Gautier V, Gonzalez-de-Peredo A, Monsarrat B, Girard J-P, et al. IL-33 is processed into mature bioactive forms by neutrophil elastase and cathepsin G. Proc Natl Acad Sci USA 2012; 109:1673-1678.
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28. Byers DE. Defining the roles of IL-33, thymic stromal lymphopoietin, and IL-25 in human asthma. Am J Respir Crit Care Med 2014; 190:715-716.
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29. Wallner M, Pichler U, Ferreira F. Recombinant allergens for pollen immunotherapy. Immunotherapy 2013; 5:1323-1338.
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30. Wiedermann U, Jahn-Schmid B, Bohle B, Renz H, Kraft D, Ebner C. Suppression of antigen-specific T-and B-cell responses by intranasal or oral administration of recombinant bet v 1, the major birch pollen allergen, in a murine model of type I allergy. J Allergy Clin Immunol 1999; 103:1202-1210.
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31. Ahmadiafshar A, Taymourzadeh B, Shaikhi A, Mazloomzadeh S, Torabi Z. Evaluation of IL10, TGF-B and Specific IgE and IgG Levels during Sublingual Rye Grass Immunotherapy. J Allergy Ther 2013; 4: 132.
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32. Allam J-P, Novak N. Immunological mechanisms of sublingual immunotherapy. Curr Opin Allergy Clin Immunol 2014; 14:564-569.
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33
34. Comer BS, Ba M, Singer CA, Gerthoffer WT. Epigenetic targets for novel therapies of lung diseases. Pharmacol Ther 2015; 147:91-110.
34
ORIGINAL_ARTICLE
Protective effects of an interaction between vagus nerve and melatonin on gastric ischemia/reperfusion: the role of oxidative stress
Objectives:Vagal pathways in gastrointestinal tract are the most important pathways that regulate ischemia/reperfusion (I/R). Gastrointestinal tract is one of the important sources of melatonin production. The aim of this study was to investigate probable protective effect of the interaction between vagus nerve and melatonin after I/R. Materials and methods:This study was performed in male rats that were divided into six groups. Cervical vagus nerve was cut bilaterally after induction of I/R and the right one was stimulated by stimulator. Melatonin or vehicle was injected intraperitoneally. The stomach was removed for histopathological and biochemical investigations. Results: A significant decrease in infiltration of gastric neutrophils and malondialdehyde (MDA) level after I/R was induced by melatonin and was disappeared after vagotomy. The stimulation of vagus nerve significantly enhanced these effects of melatonin. However, a stimulation of vagus nerve alone increased neutrophils infiltration and MDA level. Melatonin significantly increased the activities of catalase, glutathione peroxidase (GPx), superoxide dismutases (SOD). Unlike stimulation of vagus nerve, vagotomy decreased these effects of melatonin. Conclusion:According to these results, it is probable that protective effects of melatonin after I/R may be mediated by vagus nerve. Therefore, there is an interaction between melatonin and vagus nerve in their protective effects.
https://ijbms.mums.ac.ir/article_6417_7b362c139baea5a2f480535f8fb62e6e.pdf
2016-01-01
72
79
10.22038/ijbms.2016.6417
Vagus nerve
Melatonin Ischemia/reperfusion
Oxidative stress
Nader
Shahrokhi
nshahrokhsa@yahoo.com
1
Physiology Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
Mohammad
Khaksari
m_khaksari@yahoo.com
2
Endocrinology and Metabolism Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Sciences, Kerman, Iran
LEAD_AUTHOR
Shahla
Nourizad
3
Urmia University of Medical Sciences, Urmia, Iran
AUTHOR
Nava Shahrokhi
Shahrokhi
4
School of Medicine, Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
Zahra
Soltani
5
Gastroenterology and Hepatology Research Center, Institute of Basic and Clinical Physiology Sciences, Dept. of Physiology, Faculty of Medicine, Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
Ahmad
Gholamhosseinian
ghol@yahoo.com
6
Department of Biochemistry, Medical School of Afzalipour, Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
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2. Tache Y. Brainstem neuropeptides and vagus protection of the gastric mucosal against injury: role of prostaglandins, nitric oxide and calcitonin-gene related peptide in capsaicin afferents. Curr Med Chem 2012; 19:35-42.
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8. Macchi MM, Bruce JN. Human pineal physiology and functional significance of melatonin. Front Neuroendocrinol 2004; 25:177-195.
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21. Nawrot-Porabka K, Jaworek J, Leja-Szpak A, Szklarczyk J, Kot M, Mitis-Musioł M, et al. Involvement of vagus nerves in the pancreatostimulatory effects of luminal melatonin, or its precursor L-tryptophan. Study in the rats. J Physiol Pharmacol 2007; 58:81-95.
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42
ORIGINAL_ARTICLE
Vitamin D3 attenuates oxidative stress and cognitive deficits in a model of toxic demyelination
Objective(s):Multiple sclerosis (MS) is a demyelinating disease. The prevalence of MS is highest where environmental supplies of vitamin D are low. Cognitive deficits have been observed in patients with MS. Oxidative damage may contribute to the formation of MS lesions. Considering the involvement of hippocampus in MS, an attempt is made in this study to investigate the effects of vitamin D3 on behavioral process and the oxidative status in the dorsal hippocampus (CA1 area) following the induction of experimental demyelination in rats.
Materials and Methods: Animals were divided into six groups. Control group: animals received no surgery and treatment; saline group: animals received normal saline; sham group: animals received 150 μl sesame oil IP; vitamin D3 group: animals received 5 μg/kg vitamin D3 IP; lysophosphatidyl choline (LPC) group (toxic demyelination’s model): animals received LPC by stereotaxic intra-hippocampal injection of 2 μl LPC in CA1 area; Vitamin D3- treated group: animals were treated with vitamin D3 at doses of 5 μg/kg IP for 7 and 21 days post lesion. The spatial memory, biochemical parameters including catalase (CAT) activities and lipid peroxidation levels were investigated.
Results: Animals in LPC group had more deficits in spatial memory than the control group in radial arm maze. Vitamin D3 significantly improved spatial memory compared to LPC group. Also, results indicated that vitamin D3 caused a decrease in lipid peroxidation levels and an increase in CAT activities.
Conclusion: Current findings suggest that vitamin D3 may have a protective effect on cognitive deficits and oxidative stress in toxic demyelination’s model.
https://ijbms.mums.ac.ir/article_6418_a029600820831b1a01547185b3547da1.pdf
2016-01-01
80
88
10.22038/ijbms.2016.6418
Demyelination Hippocampus
Multiple Sclerosis
Oxidative stress
Vitamin D3
Sepideh
Tarbali
sepideh_tarbali@yahoo.com
1
Department of Biology, Faculty of Science, Urmia University, Urmia, Iran
AUTHOR
Shiva
Khezri
skhezri72@gmail.com
2
Department of Biology, Faculty of Science, Urmia University, Urmia, Iran
LEAD_AUTHOR
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57
ORIGINAL_ARTICLE
The effect of amniotic membrane extract on umbilical cord blood mesenchymal stem cell expansion: is there any need to save the amniotic membrane besides the umbilical cord blood?
Objective(s): Umbilical cord blood is a good source of the mesenchymal stem cells that can be banked, expanded and used in regenerative medicine. The objective of this study was to test whether amniotic membrane extract, as a rich source of growth factors such as basic-fibroblast growth factor, can promote the proliferation potential of the umbilical cord mesenchymal stem cells. Materials and Methods: The study design was interventional. Umbilical cord mesenchymal stem cells were isolated from voluntary healthy infants from hospitals in Shiraz, Iran, cultured in the presence of basic-fibroblast growth factor and amniotic membrane extracts (from pooled - samples), and compared with control cultures. Proliferation assay was performed and duplication number and time were calculated. The expression of stem cell’s specific markers and the differentiation capacity toward osteogenic and adipogenic lineages were evaluated. Results: Amniotic membrane extract led to a significant increase in the proliferation rate and duplication number and a decrease in the duplication time without any change in the cell morphology. Both amniotic membrane extract and basic-fibroblast growth factor altered the expressing of CD44 and CD105 in cell population. Treating basic-fibroblast growth factor but not the amniotic membrane extract favored the differentiation potential of the stem cells toward osteogenic lineage. Conclusion: The amniotic membrane extract administration accelerated cell proliferation and modified the CD marker characteristics which may be due to the induction of differentiation toward a specific lineage. Amniotic membrane extract may enhance the proliferation rate and duplication number of the stem cell through changing the duplication time.
https://ijbms.mums.ac.ir/article_6419_32346f61c05e2fb83961ea033733d079.pdf
2016-01-01
89
96
10.22038/ijbms.2016.6419
Amnion
Basic-fibroblast growth factor
Wharton’s jelly
Mesenchymal stem cell
Zahra
Vojdani
1
Laboratory for Stem Cell Research, Anatomy Department, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Ali
Babaei
babaeia@sums.ac.ir
2
Laboratory for Stem Cell Research, Anatomy Department, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Attiyeh
Vasaghi
3
Laboratory for Stem Cell Research, Anatomy Department, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Mojtaba
Habibagahi
4
Immunology Department, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Tahereh
Talaei-Khozani
talaeit@sums.ac.ir
5
Laboratory for Stem Cell Research, Anatomy Department, Shiraz University of Medical Sciences, Shiraz, Iran
LEAD_AUTHOR
1. Friedenstein AJ, Chailakhjan RK, Lalykina KS. The development of fibroblast colonies in monolayer cultures of guinea-pig bone marrow and spleen cells. Cell Tissue Kinet 1970; 3:393-403.
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2. Pittenger MF, Mackay AM, Beck SC, Jaiswal RK, Douglas R, Mosca JD, et al. Multilineage potential of adult human mesenchymal stem cells. Science 1999; 284:143-147.
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3.Borhani-Haghighi M, Talaei-Khozani T, Ayatollahi M, Vojdani Z. Wharton's jelly-derived mesenchymal stem cells can differentiate into hepatocyte-like cells by hepg2 cell line extract. Iran J Med Sci 2015; 40:143-151.
3
4. Ma K, Fox L, Shi G, Shen J, Liu Q, Pappas JD, et al. Generation of neural stem cell-like cells from bone marrow-derived human mesenchymal stem cells. Neurol Res 2011; 33:1083-1093.
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5. Gabr MM, Zakaria MM, Refaie AF, Ismail AM, Abou-El-Mahasen MA, Ashamallah SA, et al. Insulin-producing cells from adult human bone marrow mesenchymal stem cells control streptozotocin-induced diabetes in nude mice . Cell Transplant 2013; 22:133-145.
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6. Taghizadeh RR, Cetrulo KJ, Cetrulo CL. Wharton’s Jelly stem cells: Future clinical applications. Placenta 2011; 32:S311eS315
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10.Nguyen TH, Paluck SJ, McGahran AJ, Maynard HD. Poly (vinyl sulfonate) Facilitates bFGF-Induced Cell Proliferation. Biomacromolecules 2015; 16:2684-2692.
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12.Ramasamy R, Tong CK, Yip WK, Vellasamy S, Tan BC, Seow HF. Basic fibroblast growth factor modulates cell cycle of human umbilical cord-derived mesenchymal stem cells. Cell Prolif 2012; 45:132-139.
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14.Ponta H, Sherman L, Herrlich PA. CD44: from adhesion molecules to signaling regulators. Nat Rev Mol Cell Biol 2003; 4:33-45.
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17.Gougos A, St Jacques S, Greaves A, O'Connell PJ, d'Apice AJF, Buhring H-J, et al. Identification of distinct epitopes of endoglin, an RGD-containing glycoprotein of endothelial cells, leukemic cells, and syncytiotrophoblasts. Int Immunol 1992; 4:83-92.
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26.Dudok DV, Nagdee I, Cheung K, Liu H, Vedovelli L, Ghinelli E, et al. Effects of amniotic membrane extract on primary human corneal epithelial and limbal cells. Clin Exp Ophthalmol 2015; 43:443-448.
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27.Kordić R, Suić SP, Jandroković S, Kalauz M, Kuzman T, Skegro I, et al. Application of the amniotic membrane extract (AMX) for the persistent epithelial defect (PED) of the cornea. Coll Antropol 2013; 37:161-164.
27
28.Korzynska A, Zychowicz MA. Method of estimation of the cell doubling time on basis of the cell culture monitoring data. Biocybern Biomed Eng 2008; 28:75–82.
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31.Tauzin H, Robin S, Humbert P, Viennet C, Saas P, Courderot-Masuyer C, et al. Can leg ulcer fibroblasts phenotype be influenced by human amniotic membrane extract? Cell Tissue Bank 2014; 15:251-255.
31
32.Nakagawa H, Akita S, Fukui M, Fujii T, Akino K . Human mesenchymal stem cells successfully improve skin-substitute wound healing. Br J Dermatol 2005; 153:29-36.
32
33.Shimabukuro Y, Terashima H, Takedachi M, Maeda K, Nakamura T, Sawada K, et al. Fibroblast growth factor-2 stimulates directed migration of periodontal ligament cells via PI3K/AKT signaling and CD44/hyaluronan interaction. J Cell Physiol 2011; 226:809-821.
33
ORIGINAL_ARTICLE
Protective effect of bioactive compounds from Lonicera japonica Thunb. against H2O2-induced cytotoxicity using neonatal rat cardiomyocytes
Objective(s):Pharmacological studies showed that the extracts of Jin Yin Hua and its active constituents have lipid lowering, antipyretic, hepatoprotective, cytoprotective, antimicrobial, antibiotic, antioxidative, antiviral, and anti-inflammatory effects. The purpose of the present study was to investigate the protective effects of caffeoylquinic acids (CQAs) from Jin Yin Hua against hydrogen peroxide (H2O2)-induced and hypoxia-induced cytotoxicity using neonatal rat cardiomyocytes. Materials and Methods:Seven CQAs (C1 to C7) isolated and identified from Jin Yin Hua were used to examine the effects of H2O2-induced and hypoxia-induced cytotoxicity. We studied C4 and C6 as preventative bioactive compounds of the reactive oxygen species (ROS) production, apoptotic pathway, and apoptosis-related gene expression. Results:C4 and C6 were screened as bioactive compounds to exert a cytoprotective effect against oxidative injury. Pretreatment with C4 and C6, dose-dependently attenuated hypoxia-induced ROS production and reduced the ratio of GSSG/GStotal. Western blot data revealed that the inhibitory effect of C4 on H2O2-induced up and down-regulation of Bcl-2, Bax, caspase-3, and cleaved caspase-3. Apoptosis was evaluated by detection of DNA fragmentation using TUNEL assay, and quantified with Annexin V/PI staining. Conclusion: In vitro experiments revealed that both C4 and C6 protect cardiomyocytes from necrosis and apoptosis during H2O2-induced injury, via inhibiting the generation of ROS and activation of caspase-3 apoptotic pathway. These results demonstrated that CQAs might be a class of compounds which possess potent myocardial protective activity against the ischemic heart diseases related to oxidative stress.
https://ijbms.mums.ac.ir/article_6420_1395ece368b58ab86ccfd8ea2ee23f75.pdf
2016-01-01
97
105
10.22038/ijbms.2016.6420
Anti-apoptosis
Caffeoylquinic acids
Cardiomyocytes
Lonicera japonica Thunb
Oxidative stress
Chen
Wang
wangchencto@163.com
1
Department of Medical market, Cangzhou Central Hospital, Hebei Province, 061001, China
AUTHOR
Gang
Wang
wanggangcto@163.com
2
Department of Cardiology, Cangzhou Cardiovascular Research Institute, Cangzhou Central Hospital, Hebei Province, 061001, China
LEAD_AUTHOR
Hong
Liu
wanggangcto@126.com
3
Department of Pharmacy, General Hospital of Jixi Mining Industry Group, Heilongjiang Province, 158100, China
AUTHOR
Yun-long
Hou
4
Department of Pharmacy, Harbin Medical University, Heilongjiang Province, 150086, China
AUTHOR
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2. Giordano FJ. Oxygen, oxidative stress, hypoxia, and heart failure. J Clin Invest 2005; 115:500-508.
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4. Sun HY, Wang NP, Kerendi F, Halkos M, Kin H, Guyton RA, et al. Hypoxic postconditioning reduces cardiomyocyte loss by inhibiting ROS generation and intracellular Ca2+ overload. Am J Physiol Heart Circ Physiol 2005; 288:H1900-908.
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5. Fan H, Yang L, Fu F, Xu H, Meng Q, Zhu H, et al. Cardioprotective effects of salvianolic Acid a on myocardial ischemia-reperfusion injury in vivo and in vitro. Evid Based Complement Alternat Med 2012; 2012:508938.
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32
ORIGINAL_ARTICLE
Role of peroxisome proliferator-activated receptor alpha and gamma in antiangiogenic effect of pomegranate peel extract
Objective(s): Herbal medicines are promising cancer preventive candidates. It has been shown that Punica granatum L. could inhibit angiogenesis and tumor invasion. In this study, we investigated whether the anti-angiogenic effect of pomegranate peel extract (PPE) is partly attributable to Peroxisome proliferator-activated receptors (PPARs) activation in the Human Umbilical Vein Endothelial Cells (HUVECs). Materials and Methods: Ethanol extract from PPE was prepared. HUVECs were treated in four groups (with PPE (10 μg/ml) alone, PPE with or without PPARγ (T0070907) and α (GW6471) antagonists, and control group). The possible effect of PPARs on angiogenic regulation was checked by Matrigel assay. The mRNA expression levels of vascular endothelial growth factor (VEGF) was detected by Quantitative reverse transcription-polymerase chain reaction (QRT-PCR). Results: PPE significantly inhibited both tube formation (size, length, and junction of tubes) and VEGF mRNA expression (P<0.05). Our results showed that the anti-angiogenic effects of PPE were significantly reversed by both PPAR antagonists (P<0.05). There was no difference between PPE plus antagonists groups and the control group. Conclusion: In summary our results showed that the anti-angiogenic effects of PPE could be mediated in part through PPAR dependent pathway.
https://ijbms.mums.ac.ir/article_6421_8adfae732c5fef95f2fb68c11536f37a.pdf
2016-01-01
106
110
10.22038/ijbms.2016.6421
Angiogenesis
Peroxisome proliferator activated receptors (PPARs)
Pomegranate
Vascular Endothelial Growth Factor
Nasim
Dana
1
Applied Physiology Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Shaghayegh Haghjooy
Javanmard
sh_haghjoo@med.mui. ac.ir
2
Applied Physiology Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran
LEAD_AUTHOR
Laleh
Rafiee
3
Applied Physiology Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
1. Mund JA, Shannon H, Sinn AL, Cai S, Wang H, Pradhan KR, et al. Human proangiogenic circulating hematopoietic stem and progenitor cells promote tumor growth in an orthotopic melanoma xenograft model. Angiogenesis 2013; 16:953–962.
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4. Zarfeshany A, Asgary S, Javanmard SH. Potent health effects of pomegranate. Adv Biomed Res 2014; 3:100.
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5. Yasoubi M, Barzegar MA, Sahari MHA. Total phenolic contents and antioxidant activity of Pomegranate (Punica granatum L.) Peel Extracts. J Agric Sci Technol 2007;9:35–42.
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6. Dana N, Haghjooy Javanmard Sh RL. Inhibition of vascular endothelial growth factor-induced angiogenesis by black Pomegranate peel extract and antiproliferative effect in melanoma cell line. Res Pharm Sci 2015; 10:117-124.
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7. Jeune MAL, Kumi-Diaka J, Brown J. Anticancer activities of pomegranate extracts and genistein in human breast cancer cells. J Med Food 2005; 8:469–475.
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8. Khan GN, Gorin MA, Rosenthal D, Pan Q, Bao LW, Wu ZF, et al. Pomegranate fruit extract impairs invasion and motility in human breast cancer. Integr Cancer Ther 2009; 8:242–253.
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9. Jurenka JS. Therapeutic applications of pomegra-nate (Punica granatum L.): a review. Altern Med Rev 2008; 13:128–144.
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10. Sartippour MR, Seeram NP, Rao JY, Moro A, Harris DM, Henning SM, et al. Ellagitannin-rich pomegranate extract inhibits angiogenesis in prostate cancer in vitro and in vivo. Int J Oncol 2008; 32:475–480.
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11. Huang THW, Peng G, Kota BP, Li GQ, Yamahara J, Roufogalis BD, et al. Anti-diabetic action of Punica granatum flower extract: activation of PPAR-gamma and identification of an active component. Toxicol Appl Pharmacol 2005; 207:160–169.
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12. Hontecillas R, O’Shea M, Einerhand A, Diguardo M, Bassaganya-Riera J. Activation of PPAR gamma and alpha by punicic acid ameliorates glucose tolerance and suppresses obesity-related inflammation. J Am Coll Nutr 2009; 28:184–195.
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13. Tyagi S, Gupta P, Saini AS, Kaushal C, Sharma S. The peroxisome proliferator-activated receptor: A family of nuclear receptors role in various diseases. J Adv Pharm Technol Res 2011; 2:236–240.
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14. Woo CC, Loo SY, Gee V, Yap CW, Sethi G, Kumar AP, et al. Anticancer activity of thymoquinone in breast cancer cells: possible involvement of PPAR-γ pathway. Biochem Pharmacol 2011; 82:464–475.
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15. Biscetti F, Straface G, Pitocco D, Zaccardi F, Ghirlanda G FA. Peroxisome proliferator-activated receptors and angiogenesis. Nutr Metab Cardiovasc Dis 2009; 19:751–759.
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23. Toi M, Bando H, Ramachandran C, Melnick SJ, Imai A, Fife RS, et al. Preliminary studies on the anti-angiogenic potential of pomegranate fractions in vitro and in vivo. Angiogenesi 2003; 6:121–128.
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25. Pola R, Gaetani E, Flex A, Aprahamian TR, Bosch-Marcé M, Losordo DW, et al. Comparative analysis of the in vivo angiogenic properties of stable prostacyclin analogs: a possible role for peroxisome proliferator-activated receptors. J Mol Cell Cardiol 2004; 36:363–370.
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34
ORIGINAL_ARTICLE
Ensete superbum ameliorates renal dysfunction in experimental diabetes mellitus
Objective(s):Hyperglycemia mediated oxidative stress plays a key role in the pathogenesis of diabetic complications like nephropathy. In the present study, we evaluated the effect of ethanolic extract of Ensete superbum seeds (ESSE) on renal dysfunction and oxidative stress in streptozotocin-induced diabetic rats.
Materials and Methods:Glucose, HbA1c, total protein, albumin, renal function markers (urea, uric acid and creatinine), and lipid peroxidation levels were evaluated. Renal enzymatic and non-enzymatic antioxidants were examined along with renal histopathological study.
Results:ESSE (400 mg/kg BW t) administration reduced glucose and HbA1c, and improved serum total protein and albumin in diabetic rats. ESSE in diabetic rats recorded decrement in renal function markers and renal lipid peroxidation products along with significant increment in enzymatic and non-enzymatic antioxidants. Renal morphological abnormalities of diabetic rats were markedly ameliorated by E.superbum.
Conclusion:These results suggest that the antioxidant effect of E. superbum could ameliorate oxidative stress and delay/prevent the progress of diabetic nephropathy in diabetes mellitus.
https://ijbms.mums.ac.ir/article_6422_2cd1e0838c1e06fb69ecd69dcd88ebe1.pdf
2016-01-01
111
118
10.22038/ijbms.2016.6422
Antioxidant
Diabetes Mellitus
Diabetic nephropathy
Ensete superbum Nephroprotection
Streptozotocin
MS
Sreekutty
1
Department of Biochemistry, University of Kerala, Kariavattom, Thiruvananthapuram-695581, Kerala, India
AUTHOR
S
Mini
minisaraswathy@gmail.com
2
Department of Biochemistry, University of Kerala, Kariavattom, Thiruvananthapuram-695581, Kerala, India
LEAD_AUTHOR
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