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Ursodeoxycholic acid (UDCA) exerts antiatherogenic effects by inhibiting endoplasmic reticulum (ER) stress induced by disturbed flow

Title
Ursodeoxycholic acid (UDCA) exerts antiatherogenic effects by inhibiting endoplasmic reticulum (ER) stress induced by disturbed flow
Authors
Chung J.Kim K.H.Lee S.C.An S.H.Kwon K.
Ewha Authors
권기환정지화
SCOPUS Author ID
권기환scopus; 정지화scopus
Issue Date
2015
Journal Title
Molecules and Cells
ISSN
1016-8478JCR Link
Citation
vol. 38, no. 10, pp. 851 - 858
Keywords
AtherosclerosisDisturbed flowEndoplasmic reticulum stressEndothelial cellsUrsodeoxycholic acid
Publisher
Korean Society for Molecular and Cellular Biology
Indexed
SCI; SCIE; SCOPUS; KCI WOS scopus
Abstract
Disturbed blood flow with low-oscillatory shear stress (OSS) is a predominant atherogenic factor leading to dysfunctional endothelial cells (ECs). Recently, it was found that disturbed flow can directly induce endoplasmic reticulum (ER) stress in ECs, thereby playing a critical role in the development and progression of atherosclerosis. Ursodeoxycholic acid (UDCA), a naturally occurring bile acid, has long been used to treat chronic cholestatic liver disease and is known to alleviate endoplasmic reticulum (ER) stress at the cellular level. However, its role in atherosclerosis remains unexplored. In this study, we demonstrated the anti-atherogenic activity of UDCA via inhibition of disturbed flow-induced ER stress in atherosclerosis. UDCA effectively reduced ER stress, resulting in a reduction in expression of X-box binding protein-1 (XBP-1) and CEBP- homologous protein (CHOP) in ECs. UDCA also inhibits the disturbed flow-induced inflammatory responses such as increases in adhesion molecules, monocyte adhesion to ECs, and apoptosis of ECs. In a mouse model of disturbed flow-induced atherosclerosis, UDCA inhibits atheromatous plaque formation through the alleviation of ER stress and a decrease in adhesion molecules. Taken together, our results revealed that UDCA exerts antiatherogenic activity in disturbed flow-induced atherosclerosis by inhibiting ER stress and the inflammatory response. This study suggests that UDCA may be a therapeutic agent for prevention or treatment of atherosclerosis. © 2014 The Korean Society for Molecular and Cellular Biology.
DOI
10.14348/molcells.2015.0094
Appears in Collections:
의학전문대학원 > 의학과 > Journal papers
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