ISSN 2756-3855
International Journal of Urology and Nephrology Vol. 1 (4), pp. 040-045, December, 2013. © International Scholars Journals
Full Length Research Paper
Endothelial protein C receptor in renal tubular epithelial cells and influencing factors
Guoyuan Lu1*#, Yanping Shen1#, Wenjuan Qian2, Lei Shen1, Qing Qiao1, Ming Li1 and Zhaoyue Wang3
1Department of Nephrology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, China.
2Department of Nephrology, Zhangjiagang First People’s Hospital, Zhangjiagang, Jiangsu 215600, China.
3Department of Thrombosis and Haemostasis, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, China.
*Corresponding author. E-mail: [email protected].
Accepted 5 May, 2013
Abstract
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.
Key words: Endothelial protein C receptor, renal tubular epithelial cell, troglitazone, tumor necrosis factor-α, interleukin-1β; high glucose.