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Coxsackievirus and adenovirus receptor mediates the responses of endothelial cells to fluid shear stress

Title
Coxsackievirus and adenovirus receptor mediates the responses of endothelial cells to fluid shear stress
Authors
Chung, JihwaKim, Kyoung HwaAn, Shung HyunLee, SunmiLim, Byung-KwanKang, Sang WonKwon, Kihwan
Ewha Authors
강상원권기환정지화
SCOPUS Author ID
강상원scopus; 권기환scopus; 정지화scopus
Issue Date
2019
Journal Title
EXPERIMENTAL AND MOLECULAR MEDICINE
ISSN
1226-3613JCR Link

2092-6413JCR Link
Citation
EXPERIMENTAL AND MOLECULAR MEDICINE vol. 51
Publisher
NATURE PUBLISHING GROUP
Indexed
SCIE; SCOPUS; KCI WOS
Document Type
Article
Abstract
Endothelial mechanotransduction by fluid shear stress (FSS) modulates endothelial function and vascular pathophysiology through mechanosensors on the cell membrane. The coxsackievirus and adenovirus receptor (CAR) is not only a viral receptor but also a component of tight junctions and plays an important role in tissue homeostasis. Here, we demonstrate the expression, regulatory mechanism, and role of CAR in vascular endothelial cells (ECs) under FSS conditions. Disturbed flow increased, whereas unidirectional laminar shear stress (LSS) decreased, CAR expression in ECs through the Kruppel-like factor 2 (KLF2)/activator protein 1 (AP-1) axis. Deletion of CAR reduced the expression of proinflammatory genes and endothelial inflammation induced by disturbed flow via the suppression of NE-kappa B activation. Consistently, disturbed flow-induced atherosclerosis was reduced in EC-specific CAR KO mice. CAR was found to be involved in endothelial mechanotransduction through the regulation of platelet endothelial cell adhesion molecule 1 (PECAM-1) phosphorylation. Our results demonstrate that endothelial CAR is regulated by FSS and that this regulated CAR acts as an important modulator of endothelial mechanotransduction by FSS.
DOI
10.1038/s12276-019-0347-7
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자연과학대학 > 생명과학전공 > Journal papers
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