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Renal-Electrolyte and Hypertension Division, Department of Medicine, and the Penn Center for the Molecular Studies of Kidney Diseases, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6144
The core protein
of the proteoglycan decorin binds and neutralizes transforming growth
factor-
(TGF-). Activation of TGF- is crucial to tissue injury
in diabetic nephropathy, but it is not currently known whether decorin
plays a role in this disease. Mouse kidney cortex demonstrates more
than a twofold increase in decorin mRNA after 1, 2, 3, and 6 wk of
streptozotocin diabetes. Various mouse and rat renal cell types are
studied in culture under normal or high-glucose conditions. Mouse
glomerular mesangial and proximal tubular epithelial cells
constitutively express decorin, and high glucose (450 mg/dl) increases
decorin mRNA fourfold compared with 100 mg/dl glucose. Unlike rat
mesangial cells, rat glomerular epithelial and endothelial cells do not
constitutively express decorin, and no induction is observed in high
glucose. When mouse mesangial and proximal tubular cells are exposed to
TGF-1 (1 ng/ml), decorin mRNA is significantly decreased. Our
findings suggest that the increased decorin expression in the diabetic kidney may counteract the hypertrophic and prosclerotic effects of
increased TGF- levels and that a negative feedback loop may exist
between decorin and TGF-.
transforming growth factor-; diabetic nephropathy; glomerulus; endothelium; epithelium; rat
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