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Fluid shear stress regulates the expression of Lectin-like oxidized low density lipoprotein receptor-1 via KLF2-AP-1 pathway depending on its intensity and pattern in endothelial cells

Title
Fluid shear stress regulates the expression of Lectin-like oxidized low density lipoprotein receptor-1 via KLF2-AP-1 pathway depending on its intensity and pattern in endothelial cells
Authors
Lee, Ji YoonChung, JihwaKim, Kyoung HwaAn, Shung HyunKim, MinsukPark, JunbeomKwon, Kihwan
Ewha Authors
권기환김민석박준범
SCOPUS Author ID
권기환scopus; 김민석scopus; 박준범scopus
Issue Date
2018
Journal Title
ATHEROSCLEROSIS
ISSN
0021-9150JCR Link

1879-1484JCR Link
Citation
ATHEROSCLEROSIS vol. 270, pp. 76 - 88
Keywords
Fluid shear stressVascular endothelial cellsLOX-1Mechanosensory complexKruppel-like factor 2Activator protein-1
Publisher
ELSEVIER IRELAND LTD
Indexed
SCI; SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
Background and aims: Vascular endothelial cells (ECs) are exposed to fluid shear stress (FSS), which modulates vascular pathophysiology. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is crucial in endothelial dysfunction and atherosclerosis. We elucidated the mechanism regulating LOX-1 expression in ECs by FSS. Methods: Human umbilical vein endothelial cells were exposed to laminar shear stress (LSS) of indicated intensities using a unidirectional steady flow, or to oscillatory shear stress (OSS) using a bidirectional disturbed flow. In vivo studies were performed in a mouse model of partial carotid ligation and human pulmonary artery sections. Results: Within ECs, OSS upregulated LOX-1 expression, while LSS (20 dyne/cm(2)) downregulated it. We confirmed that OSS-induced LOX-1 expression was suppressed when the mechanotransduction was inhibited by knockdown of the mechanosensory complex. In addition, we demonstrated that Kruppellike factor 2 (KLF2) has an inhibitory role on OSS-induced LOX-1 expression. Next, we determined that activator protein-1 (AP-1) was the key transcription factor inducing LOX-1 expression by OSS, which was inhibited by KLF2 overexpression. To explore whether the intensity of LSS affects LOX-1 expression, we tested three different intensities (20, 60, and 120 dyne/cm(2)) of LSS. We observed higher LOX-1 expression with high shear stresses of 120 dyne/cm(2) compared to 20 and 60 dyne/cm(2), with OSS-like KLF2-AP-1 signaling patterns. Furthermore, ECs within disturbed flow regions showed upregulated LOX-1 expression in vivo. Conclusions: We concluded that LOX-1 expression on ECs is regulated via FSS depending on its intensity as well as pattern. Furthermore, this is mediated through the KLF2-AP1 pathway of mechanotransduction. (C) 2018 Elsevier B.V. All rights reserved.
DOI
10.1016/j.atherosclerosis.2018.01.038
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의과대학 > 의학과 > Journal papers
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