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Articles in PresS, published online ahead of print October 15, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.00189.2001
Submitted on June 22, 2001
Accepted on September 28, 2001
Activation
1 Departmetn of Medicine, University of Miami, School of Medicine, Miami, FL, USA
2 Division of Nephrology and Hypertension, Vanderbilt University Medical Center, Vanderbilt, TN, USA
* To whom correspondence should be addressed. E-mail: fzheng{at}med.miami.edu.
We found that PPAR mRNA was reduced by 77% in glomeruli of diabetic mice. Since mesangial cells play an important role in diabetic nephropathy, we examined the regulation of type I collagen expression by PPAR and TGF- ß1 in mouse mesangial cells in the presence of 6 mM and 25 mM glucose. Mesangial cells contained functionally active PPAR. Exposure to 25 mM glucose resulted in reduced PPAR expression and transcriptional activity, accompanied by increased type I collagen expression. Restoration of PPAR expression to normal levels in cells cultured in 25 mM glucose, by transfection with a PPAR expression construct, returned type I collagen levels toward normal values. Activation of PPAR by an agonist also decreased type I collagen mRNA, and blocked TGF- ß1 mediated upregulation of type I collagen mRNA and protein. Moreover, PPAR activation suppressed both basal and activated TGF- ß1 responses in mesangial cells. PPAR suppressed TGF- ß1 transcriptional activity. This action which was blocked by transfection of cells with a dominant negative PPAR construct. In summary, PPAR blocks the increased type I collagen mRNA and protein expression mediated by TGF- ß1 in mesangial cells.
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