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 PPARalpha activation abolishes LDL effects in human aortic SMCs (hAoSMCs). Herein is the first report of PPARgamma activation by troglitazone (TG) exerting its inhibitory effects on LDL-induced cell proliferation via generation not of H(2)O(2), but of O2(.-), and the subsequent activation of Erk1/2 in hAoSMCs. Moreover, in this study TG abolished the LDL-accelerated G(1)-S progression to control levels via down-regulation of active cyclinD1/CDK4 and cyclinE/CDK2 complexes and up-regulation of p21(Cip1) 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(.-) is located at the crossroads between LDL signaling and cell proliferation.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Heo KS,Kim DU,Ryoo S,Nam M,Baek ST,Kim L,Park SK,Myung CS,Hoe KLdoi
10.1016/j.bbrc.2007.06.006subject
Has Abstractpub_date
2007-08-10 00:00:00pages
1017-23issue
4eissn
0006-291Xissn
1090-2104pii
S0006-291X(07)01231-4journal_volume
359pub_type
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