Thiazolidinediones inhibit TNFα induction of PAI-1 independent of PPARγ activation

被引：42
作者：
Liu, HB
Hu, YS
Medcalf, RL
Simpson, RW
Dear, AE
机构：
[1] Monash Univ, Australian Ctr Blood Dis, Melbourne, Vic 3181, Australia
[2] Monash Univ, Div Biotechnol, Eastern Clin Res Unit, Melbourne, Vic 3181, Australia
[3] Box Hill Hosp, Dept Endocrinol & Diabet, Melbourne, Vic 3128, Australia
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2005年 / 334卷 / 01期
关键词：
tumour necrosis factor alpha; plasminogen activator inhibitor type-1; thiazolidinedione; peroxisome proliferator-activated receptor gamma;
D O I：
10.1016/j.bbrc.2005.06.055
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Increased plasminogen activator inhibitor type I (PAI-1) levels are observed in endothelial cells stimulated by tumour necrosis factor alpha (TNF alpha). Thiazolidinediones (TZDs) may inhibit elevated endothelial cell PAI-1 accounting, in part, for the putative atheroprotective effects of TZDs. In an endothelial cell line, Rosiglitazone (RG) and Pioglitazone (PG) inhibited induction of PAI-1 by TNF alpha. The specific peroxisome proliferator-activated receptor gamma (PPAR gamma) inhibitor, SR-202, failed to modulate this effect. RG also inhibited the effect of TNF alpha on a reporter gene construct harbouring the proximal PAI-1 promoter and PAI-1 mRNA in cells cotransfected with a dominant-negative PPAR-gamma construct. RG and PG attenuated TNF alpha-mediated induction of trans-acting factor(s) Nur77/Nurr1 and binding of nuclear proteins (NP) to the cis-acting element (NBRE). SR-202 failed to modulate these effects. The observations suggest TZDs inhibit TNF alpha-mediated PAI-1 induction independent of inducible PPAR gamma activation and this may involve in the modulation of Nur77/Nurr1 expression and NP binding to the PAI-1 NBRE. (c) 2005 Elsevier Inc. All rights reserved.
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收藏
页码：30 / 37
页数：8
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