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- W2006367961 abstract "The peroxisome proliferator-activated receptor gamma activating compounds thiazolidinedione (TZD) have been shown to inhibit diabetes-induced glomerular transforming growth factor-beta1 (TGF-beta1) expression, thereby ameliorating diabetic nephropathy. Here we examined the hypothesis that TZDs block high glucose-induced TGF-beta1 gene activation by interaction with the activated protein kinase C-c-Fos-TGF-beta1 promoter cascade in mesangial cells. The TZD compounds troglitazone and rosiglitazone completely prevented the high glucose induction of both TGF-beta1 promoter activity and elevation in nuclear c-Fos protein levels. The scavenging properties of troglitazone were shown not to be responsible for this inhibitory action, because hydrogen peroxide-mediated stimulation of TGF-beta1 promoter activity was not blocked. TZD-treatment did not interfere with the transcriptional activity of c-Fos responsible for stimulation of the TGF-beta1 promoter. The findings suggest a molecular mechanism by which TZD-treatment reduces specifically high glucose-induced, c-Fos-mediated gene activation, since phorbol ester-induced c-Fos mRNA and protein expression and subsequent elevation of TGF-beta1 mRNA expression were not prevented by TZDs." @default.
- W2006367961 created "2016-06-24" @default.
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- W2006367961 date "2003-05-01" @default.
- W2006367961 modified "2023-10-12" @default.
- W2006367961 title "c-Fos-driven transcriptional activation of transforming growth factor β-1: inhibition of high glucose-induced promoter activity by thiazolidinediones" @default.
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- W2006367961 doi "https://doi.org/10.1016/s0006-291x(03)00599-0" @default.
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