Hyperbaric environment up-regulates CD15s expression on leukocytes, down-regulates CD77 expression on renal cells and up-regulates CD34 expression on pulmonary and cardiac cells in rat

Document Type : Original Article

Authors

1 Postgraduate Student at University of Split School of Medicine, Split, Croatia

2 Department of Medical Chemistry and Biochemistry, University of Split School of Medicine, Split, Croatia

3 Faculty of Kinesiology, University of Split, Split, Croatia

4 Department of Medical Biology, University of Split School of Medicine, Split, Croatia

Abstract

Objective(s): The aim of this study was to estimate effects of hyperbaric (HB) treatment by determination of CD15s and CD11b leukocyte proinflammatory markers expression.  In addition, this study describes changes in CD77 and CD34 expression on rat endothelial cells in renal, pulmonary and cardiac tissue following exposure to hyperbaric pressure.
Materials and Methods:Expression of CD11b and CD15s on leukocytes, as well as CD77 and CD34 expression on endothelial cells in cell suspensions of renal, pulmonary and cardiac tissue in rats after hyperbaric treatment and in control rats were determined by flow cytometry.
Results: Hyperbaric treatment significantly increased percentage of leukocytes expressing CD15s+CD11b- (from 1.71±1.11 to 23.42±2.85, P<0.05). Hyperbaric treatment significantly decreased sum percentage of CD77+CD34- and CD77+CD34+ renal cells (from 16.35±5.5 to 4.48 ±1.28, P<0.05). Hyperbaric treatment significantly increased percentage of CD34+ pulmonary cells (from 3.27±2.01 to 11.92±6.22, P<0.05). Our study is the first reporting the hyperbaric environment influence on CD34+ heart cells in rats.
Conclusion:The current findings of increased percentage of leukocytes expressing endothelial selectin ligand CD15s after hyperbaric treatment, point its role in endothelial damage prevention. We found out a significantly increase in percentage of CD34+ cardiac cells as well as CD34+ pulmonary cells in rats after HB treatment which could be a part of repair mechanism of injured endothelium caused by hyperoxia.

Keywords

References

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Iranian Journal of Basic Medical Sciences
Volume 19, Issue 8
August 2016
Pages 821-828

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