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activity is
associated with renal microvasculature
1 Division of Nephrology, Department of Medicine, and Departments of 3 Molecular Physiology and Biophysics and 2 Pharmarcology, Vanderbilt University Medical Center, Nashville, Tennessee 37212
First published July 12, 2001;
10.1152/ajprenal.00025.2001.
Peroxisome proliferator-activated
receptor-
(PPAR) is a nuclear transcription factor and the
pharmacological 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 that 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,
adipocyte fatty acid-binding protein (A-FABP), in renal glomerular
cells and renal medullary microvascular endothelial cells, demonstrated
by both 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 MC PPAR can also drive PPAR reporter. Troglitazone and
15-deoxy-
12,14 prostaglandin J2 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 pharmacological target to directly modulate glomerular injury.
glomeruli; mesangial cell; adipocyte fatty acid-binding protein
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