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Cytosolic Hsp60 orchestrates the survival and inflammatory responses of vascular smooth muscle cells in injured aortic vessels

Title
Cytosolic Hsp60 orchestrates the survival and inflammatory responses of vascular smooth muscle cells in injured aortic vessels
Authors
Choi, BoaeChoi, MinaPark, CharnyLee, Eun KyungKang, Dong HoonLee, Doo JaeYeom, Jae YoonJung, YeonjooKim, JaesangLee, SanghyukKang, Sang Won
Ewha Authors
이상혁강상원김재상이두재정연주강동훈
SCOPUS Author ID
이상혁scopus; 강상원scopus; 김재상scopus; 이두재scopus; 정연주scopus; 강동훈scopus
Issue Date
2015
Journal Title
CARDIOVASCULAR RESEARCH
ISSN
0008-6363JCR Link1755-3245JCR Link
Citation
vol. 106, no. 3, pp. 498 - 508
Keywords
Hsp60Vascular smooth muscle cellsNF-kappa BInflammationRestenosis
Publisher
OXFORD UNIV PRESS
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Aims Pro-inflammatory response of vascular smooth muscle cells (VSMCs) is triggered by endothelial damage and a causative step for thrombosis and neointimal thickening in the injured arterial vessels. Therefore, we investigate a role of cytosolic Hsp60 as a novel pro-inflammatory mediator in VSMCs. Methods and results Hsp60 was detected in the cytosol of VSMCs. The selective depletion of cytosolic Hsp60 in VSMCs reduced the I kappa B kinase activation, repressed the induction of nuclear factor (NF)-kappa B-dependent survival genes (MnSOD and Bfl-1/A1), and enhanced apoptotic death in response to TNF-alpha Moreover, a quantitative RNA sequencing revealed that the expression of 75 genes among the 774 TNF-alpha-inducible genes was significantly reduced by the depletion of cytosolic Hsp60. In particular, the expression of pro-inflammatory cytokines/chemokines, such as CCL2, CCL20, and IL-6, was regulated by the cytosolic Hsp60 in VSMCs. Finally, the depletion of cytosolic Hsp60 markedly inhibited the neointimal thickening in the balloon-injured arterial vessels by inducing apoptotic cell death and inhibiting chemokine production. Conclusions This study provides the first evidence that cytosolic Hsp60 could be a therapeutic target for preventing VSMC hyperplasia and inflammatory response in the injured vessels.
DOI
10.1093/cvr/cvv130
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자연과학대학 > 생명과학전공 > Journal papers
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