Increased decorin mrna in diabetic mouse kidney and in mesangial
and tubular cells cultured in high glucose.
Mogyorosi, Andras, and Fuad N. Ziyadeh.
Renal-Electrolyte and Hypertension Division, Department of
Medicine, and the Penn Center for the Molecular Studies of Kidney
Diseases, University of Pennsylvania, Philadelphia, Pennsylvania,
USA
APStracts 5:0145F, 1998.
The core protein of the proteoglycan decorin binds and neutralizes
transforming growth factor-b (TGF-b). Activation of TGF-b 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 two-fold increase in decorin mRNA after
1, 2, 3, and 6 weeks 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 four-fold as 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-b1 (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-b levels and
that a negative feedback loop may exist between decorin and TGF-b.
Received 7 April 1998; accepted in final form 13 August 1998.
APS Manuscript Number F81-8.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 21 September 1998