AP-1 complexes mediate oxidized LDL-induced overproduction of TGF-beta(1) in rat mesangial cells.

AP-1 complexes mediate oxidized LDL-induced overproduction of TGF-beta(1) in rat mesangial cells. Research Abstract Details 

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AP-1 complexes mediate oxidized LDL-induced overproduction of TGF-beta(1) in rat mesangial cells. Abstract Text:

Zhaolong Wu,Qin Zhou,Yang Lan,Yuancheng Wang,Xunhui Xu,Huiming Jin,

Oxidized Low Density Lipoprotein (Ox-LDL)-induced overproduction of the prosclerotic cytokine transforming growth factor-beta1 (TGF-beta(1)) has been implicated in the pathogenesis of renal fibrosis and sclerosis. Because Ox-LDL increases TGF-beta(1) mRNA levels in rat mesangial cells, our investigation was designed to characterize these effects on the rat TGF-beta(1) promoter activity. We transfected luciferase reporter gene constructs containing TGF-beta(1) 5'-flanking sequence (from -1550 to +57 bp) into mesangial cells. By assaying progressively deleted mutations in the promoter, we found two regions that were responsible for the induction. One is a negative regulatory region (-422 to -629) which represses the transcription of the TGF-beta(1) gene, the other is a positive regulatory region (-845 to -1550) which enhances the transcription unit efficiently. There is an activating protein-1(AP-1) binding site in the latter region. Mutagenesis in the AP-1 binding sites abolished the Ox-LDL effect. Furthermore, addition of the AP-1 inhibitor curcumin obliterated the Ox-LDL response. The Ox-LDL-induced TGF-beta(1) promoter activation was also prevented by inhibitors of protein kinase C, but not by p38 mitogen-activated protein kinase. Electrophoretic mobility shift assays with oligonucleotides containing AP-1 binding sites showed that Ox-LDL treatment significantly enhanced the binding activity of nuclear proteins of mesangial cells. Supershift assays demonstrated that c-Jun was present in the protein-DNA complexes under stimulation of Ox-LDL. The functional and structural results show that Ox-LDL regulates rat TGF-beta(1) gene expression through AP-1 binding sites and gives rise to the involvement of protein kinase C in Ox-LDL-induced TGF-beta(1) gene expression.

AP-1 complexes mediate oxidized LDL-induced overproduction of TGF-beta(1) in rat mesangial cells. Publishing Authors By Initials

Z Wu,Q Zhou,Y Lan,Y Wang,X Xu,H Jin,

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PUBMED ID PMID:

MEDLINE DATE: 2004 Jul-Aug

AP-1 complexes mediate oxidized LDL-induced overproduction of TGF-beta(1) in rat mesangial cells. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Cell biochemistry and function

VOLUME: 22

Page Numbers: 237-47

Journal Abbreviation: Cell Biochem. Funct.

ISSN: 0263-6484

DAY: 12

MONTH: 07

YEAR: 2004

AP-1 complexes mediate oxidized LDL-induced overproduction of TGF-beta(1) in rat mesangial cells. Information

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LANGUAGE: eng

NlmUniqueID: 8305874

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Grant and Affiliation Information for AP-1 complexes mediate oxidized LDL-induced overproduction of TGF-beta(1) in rat mesangial cells.

AFFILIATION: Division of Nephrology, Zhongshan Hospital, Shanghai Medical College of Fudan University, Shanghai, P.R. China. professor-wu@yahoo.com.cn

Country: England

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MEDLINETA: Cell Biochem Funct

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