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CD137 (4-1BB) deficiency reduces atherosclerosis in hyperlipidemic mice

Title
CD137 (4-1BB) deficiency reduces atherosclerosis in hyperlipidemic mice
Authors
Jeon H.J.Choi J.-H.Jung I.-H.Park J.-G.Lee M.-R.Lee M.-N.Kim B.Yoo J.-Y.Jeong S.-J.Kim D.-Y.Park J.E.Park H.-Y.Kwack K.Choi B.K.Kwon B.S.Oh G.T.
Ewha Authors
오구택이미니
SCOPUS Author ID
오구택scopus; 이미니scopusscopus
Issue Date
2010
Journal Title
Circulation
ISSN
0009-7322JCR Link
Citation
vol. 121, no. 9, pp. 1124 - 1133
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Background: The tumor necrosis factor receptor superfamily, which includes CD40, LIGHT, and OX40, plays important roles in atherosclerosis. CD137 (4-1BB), a member of the tumor necrosis factor receptor superfamily, has been reported to be expressed in human atherosclerotic lesions. However, limited information is available on the precise role of CD137 in atherosclerosis and the effects of blocking CD137/CD137 ligand signaling on lesion formation. Methods and results: We generated CD137-deficient apolipoprotein E-knockout mice (ApoECD137) and LDL-receptor-knockout mice (LdlrCD137) to investigate the role of CD137 in atherogenesis. The deficiency of CD137 induced a reduction in atherosclerotic plaque lesions in both atherosclerosis mouse models, which was attributed to the downregulation of cytokines such as interferon-γ, monocyte chemoattractant protein-1, and tumor necrosis factor-α. CD137 signaling promoted the production of inflammatory molecules, including monocyte chemoattractant protein-1, interleukin-6, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1, in endothelial cells. Stimulation of CD137 ligand signaling activated monocytes/macrophages and augmented the production of proinflammatory cytokines in atherosclerotic vessels. Conclusions: CD137/CD137 ligand signaling plays multiple roles in the progression of atherosclerosis, and thus, blockade of this pathway is a promising therapeutic target for the disease. Copyright © 2010 American Heart Association. All rights reserved.
DOI
10.1161/CIRCULATIONAHA.109.882704
Appears in Collections:
자연과학대학 > 생명과학전공 > Journal papers
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