상세 정보

underline
Metadata Downloads : dc(xml) or Excel
Cited 0 time in scopus ci

Title 

PPARγ activation abolishes LDL-induced proliferation of human aortic smooth muscle cells via SOD-mediated down-regulation of superoxide

Authors 

Kyung Sun HeoDong Uk KimS RyooMiyoung NamSeung Tae BaekL KimSong Kyu ParkC S MyungKwang Lae Hoe

Publisher 

Elsevier

Issue Date 

2007

Citation 

Biochemical and Biophysical Research Communications, vol. 359, no. 4, pp. 1017-1023

Keywords 

atherosclerosislow-density lipoproteinsMAP kinasePPARsmooth muscle cellsuperoxidetroglitazonesuperoxide dismutasecell cycle G1 phase

Abstract 

Native LDL would be a mitogenic and chemotactic stimulus of VSMC proliferation and differentiation in the atherosclerotic lesion where endothelial disruption occurred. In previous studies, our group investigated the molecular mechanisms by which LDL induces IL-8 production and by which PPARα activation abolishes LDL effects in human aortic SMCs (hAoSMCs). Herein is the first report of PPARγ activation by troglitazone (TG) exerting its inhibitory effects on LDL-induced cell proliferation via generation not of H2O2, but of O2{radical dot} -, and the subsequent activation of Erk1/2 in hAoSMCs. Moreover, in this study TG abolished the LDL-accelerated G1-S progression to control levels via down-regulation of active cyclinD1/CDK4 and cyclinE/CDK2 complexes and up-regulation of p21Cip1 expression. TG exerted its anti-proliferative effects through the up-regulation of basal superoxide dismutase (SOD) expression. This data suggests that the regulation of O2{radical dot} - is located at the crossroads between LDL signaling and cell proliferation.

ISSN 

0006-291X

Link 

http://dx.doi.org/10.1016/j.bbrc.2007.06.006

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


There are no files associated with this item.
qrcode

FusionCharts.
DSpace Software Coptright(c) 2010 MIT and Hewleft-Packard  /  KRIBB-REPOSITORY ( Email:jakim@kribb.re.kr)