Circulating endothelial cell protein C receptor: Endothelial regulation and cumulative impact of gender and A3 haplotype

9Citations
Citations of this article
11Readers
Mendeley users who have this article in their library.
Get full text

Abstract

Background: The endothelial cell (EC) protein C receptor (EPCR) negatively regulates coagulation and inflammation. Factors and mechanisms regulating the expression of cell-bound EPCR and the release of soluble (s) EPCR are still unclear. Methods: We investigated the reciprocal regulation of membrane-bound and sEPCR upon inflammation using primary cultures of vascular EC. The impact of 2 parameters, gender and EPCR gene A3 haplotype, on sEPCR plasma basal level and endothelial expression was examined by Elisa and flow cytometry. Results: Exposure of EC to tumor necrosis factor α causes a rapid downregulation of membrane-associated EPCR expression without affecting markedly the spontaneous release of sEPCR by EC. In a cohort of 100 healthy donors, we show that males express significantly higher basal sEPCR in plasma than females (194 ± 12 vs. 145 ± 9 ng/ml, respectively, p < 0.01). Both gender and EPCR A3 haplotype affect sEPCR plasma levels but have no apparent effect on EPCR expression by EC. No quantitative correlation between cellular expression and circulating blood sEPCR was observed, suggesting that endothelial expression may not reflect the plasma level. Conclusion: Male gender is another parameter with A3 haplotype associated with elevated sEPCR levels in blood, and both parameters may contribute to selective regulatory mechanisms of EPCR release upon inflammation. Copyright © 2011 S. Karger AG.

Cite

CITATION STYLE

APA

Guitton, C., Gérard, N., Quillard, T., & Charreau, B. (2011). Circulating endothelial cell protein C receptor: Endothelial regulation and cumulative impact of gender and A3 haplotype. Journal of Vascular Research, 48(4), 336–346. https://doi.org/10.1159/000322582

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free