EPAC1 promotes adaptive responses in human arterial endothelial cells subjected to low levels of laminar fluid shear stress: Implications in flow-related endothelial dysfunction
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- 作者：Sarah N. Rampersada ; Silja I. Freitagb ; Fabien Hubertb ; Paulina Brzezinskab ; Nathalie Butlerb ; M. Bibiana Umanab ; Alie R. Wudwuda ; Donald H. Mauricea ; b ; mauriced@queensu.ca" class="auth_mail" title="E-mail the corresponding author
- 关键词：AJ ; adherens junction ; CREB ; cAMP response element binding protein ; eNOS ; endothelial nitric oxide synthase ; EPAC ; exchange protein activated by cAMP ; FSS ; fluid shear stress ; HAEC ; human arterial endothelial cell ; KLF2 ; Krü ; ppel-like factor 2 ; PDE ; phosphodiesterase ; PECAM-1 ; platelet endothelial cell adhesion molecule ; PKA ; protein kinase A ; TM ; thrombomodulin ; VASP ; vasodilator-stimulated phosphoprotein ; VEC ; vascular endothelial cell ; VECAD ; vascular endothelial cadherin ; VEGFR2 ; vascula
- 刊名：Cellular Signalling
- 出版年：2016
- 出版时间：June 2016
- 年：2016
- 卷：28
- 期：6
- 页码：606-619
- 全文大小：2609 K
文摘
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EPAC1 activation enhances HAEC alignment and elongation under low FSS.
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Knockdown of EPAC1 impairs HAEC morphological adaptations to low FSS and reduces the expression of flow-dependent genes.
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EPAC1 mediates PECAM1/VEGFR2/VECAD mechanosensory complex assembly in HAECs.
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VEGFR2 mechanosensor signaling to AKT is impaired in cells with reduced EPAC1 levels.