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Papers In Press, published online ahead of print April 27, 2003
Department of Medicine D, University of Muenster, Muenster 48149
Corresponding Author: schaefl{at}uni-muenster.de
During glomerular inflammation mesangial cells are the major source and target of nitric oxide which profoundly influences proliferation, adhesion and death of mesangial cells. The effect of nitric oxide on the mRNA expression pattern of cultured rat mesangial cells was therefore investigated by RNA-arbitrarily-primed polymerase chain reaction. Employing this approach, biglycan expression turned out to be down-regulated time- and dose-dependently either by interleukin-1ß-stimulated endogenous nitric oxide production or by direct application of the exogenous nitric oxide donor, diethylenetriamine nitric oxide. There was a corresponding decline in the rate of biglycan biosynthesis and in the steady state level of this proteoglycan. In vivo, in a model of mesangioproliferative glomerulonephritis upregulation of inducible nitric oxide synthase mRNA was associated with reduced expression of biglycan in isolated glomeruli. Biglycan expression could be normalized, both in vitro and in vivo, by using a specific inhibitor of the inducible nitric oxide synthase, L-N6-(l-iminoethyl) L-lysine dihydrochloride. Further studies showed that biglycan inhibited cell adhesion on type I collagen and fibronectin due to its binding to these substrates. More importantly, biglycan protected mesangial cells from apoptosis by decreasing caspase-3 activity, and it counteracted the proliferative effects of PDGF-BB. These findings indicate a signalling role of biglycan and describe a novel pathomechanism by which nitric oxide modulates the course of renal glomerular disease through regulation of biglycan expression.
J. Biol. Chem, 10.1074/jbc.M210574200
Submitted on October 16, 2002
Revised on April 27, 2003
Accepted on April 27, 2003
Biglycan, a nitric oxide-regulated gene, affects adhesion, growth and survival of mesangial cells
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