Resistin impairs activation of protein C by suppressing EPCR and increasing SP1 expression - 09/12/18
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Highlights |
• | Resistin inhibits thrombin induced protein C activation. |
• | Resistin reduces the expression of EPCR but not TM in HUVECs, mediated by SP1. |
• | Blockage of SP1 abolished the effects of Resistin on protein C activation. |
Abstract |
Endothelial cells are vital to blood coagulation and maintain whole body hemostasis. Binding of endothelial cells to endothelial protein C receptor (EPCR) and thrombomodulin (TM) is essential to the formation of activated protein C (APC), one of the key factors regulating blood coagulation. In our study, we showed that resistin, an adipocyte hormone, suppresses thrombin-induced protein C activation in endothelial cells. Resistin treatment results in a reduction in EPCR expression, but not TM. Mechanistically, we demonstrate that resistin induces expression of the nuclear transcription factor SP-1, which could lead to downregulation of EPCR. Both inhibition and silencing of SP1 protein abolishes abnormal APC generation induced by resistin. Collectively, our data support a new role of resistin in disturbing APC formation.
Le texte complet de cet article est disponible en PDF.Keywords : Resistin, Activated protein C, EPCR, SP1, HUVEC
Plan
Vol 109
P. 930-937 - janvier 2019 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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