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Articles in PresS, published online ahead of print July 12, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.0025.2001
Submitted on January 31, 2001
Accepted on July 5, 2001
(PPAR) activity is associated with renal microvasculature
1 Medicine/Nephrology, Vanderbilt University Medical Center, Nashville, TN, USA
2 Medicine/Nephrology, Vanderbilt University Medical Center, Nashville, TN, USA; Pharmacology, Vanderbilt University Medical Center, Nashville, TN, USA
3 Medicine/Nephrology, Vanderbilt University Medical Center, Nashville, TN, USA; Mol. Physiol. & Biophys., Vanderbilt University Medical Center, Nashville, TN, USA
* To whom correspondence should be addressed. E-mail: youfei.guan{at}mcmail.vanderbilt.edu.
PPAR is a nuclear transcription factor and the pharmacologic target for antidiabetic thiazolidinediones (TZDs). TZDs ameliorate diabetic nephropathy and have direct effects on cultured mesangial cells (MCs), however in situ hybridization failed to detect expression of PPAR in glomeruli in vivo. The purpose of this study was to determine whether PPAR is expressed in renal glomeruli. Two rabbit PPAR isoforms were cloned. Nuclease protection assays demonstrate both PPAR isoforms are expressed in freshly isolated glomeruli. Treatment of rabbits with the TZD, troglitazone, selectively induced expression of an endogenous PPAR target gene, A-FABP, in renal glomerular cells and renal medullary microvascular endothelial cells demonstrated both by in situ hybridization and immunostain. Troglitazone also dramatically increased A-FABP expression in cultured MCs. Constitutive PPAR expression was detected in cultured rabbit MCs. Endogenous mesangial cell PPAR can also drive PPAR reporter. Troglitazone and 15dPGJ2 at low concentrations reduced mesangial cell 3H-thymidine incorporation without affecting viability. These data suggest that constitutive PPAR activity exists in renal glomeruli in vivo and could provide a pharmacologic target to directly modulate glomerular injury.
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