This in vitro study demonstrates that EPCR is expressed in renal tubular epithelial cells and its expression is modulated by inflammatory cytokines, high glucose, and troglitazone.
May suggest troglitazone protects renal EPCR expression; animal data leaves open applicability to diabetic nephropathy.
The endothelial protein C receptor (EPCR) plays an important role within the protein C pathway in regulating coagulation and inflammation. It was reported that EPCR was expressed in large vessels, placenta, heart, liver and lung endothelial cell. However, there are a few studies concerned about renal epithelial cells. This study aims to investigate EPCR expression in renal tubular epithelial cells and related influencing factors. EPCR expression was assessed by flow cytometry in renal tubular epithelial cells. The effects of some reagents (high glucose, tumor necrosis factor–α and interleukin-1β) were measured by RT-PCR. The results showed that renal tubular epithelial cells had the high expression of EPCR level. High glucose, tumor necrosis factor–α and interleukin-1β might reduce EPCR expression. And troglitazone could significantly improve the inhibition. In conclusion, we found EPCR expression in renal tubular epithelial cells in vitro . Some factors such as high glucose, tumor necrosis factor–α and interleukin-1β can impact on EPCR. However, troglitazone had protective effects of EPCR on injured cells.
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Lu et al. (2011) studied this question.
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