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- W1574009689 abstract "Introduction Decorin, a small leucine-rich proteoglycan, participates in extracellular matrix assembly and influences cell behaviour by interacting with signalling membrane receptors and TGF-β. Treatment with decorin has been shown to have beneficial effects in an acute model of mesangioproliferative glomerulonephritis due to interaction with TGF-β. The underlying mechanisms, however, remain unclear because upon complex formation with TGF-β, the cytokine's activity may become increased, decreased or not influenced at all. Hence, the objectives of the present study were twofold: firstly, to provide evidence that decorin influences the course and final outcome of renal inflammation and secondly, to find anti-fibrotic mechanisms of decorin both related and unrelated to the regulation of TGF-β activity.Results Based on our studies in human diabetic nephropathy, we postulate two regulatory mechanisms by which decorin modulates TGF-β-mediated fibrosis: (1) increased quantities of glomerular decorin are synthesized and form complexes with TGF-β, which then are removed via glomerular capillaries or the urinary tract, and (2) in the presence of type-I collagen, decorin is able to sequester TGF-β in the extracellular matrix, thereby withdrawing the cytokine from its cell-surface receptors. Furthermore, we have compared the evolution of tubulointerstitial fibrosis in wild-type (WT) and decorin–/– mice in a model of unilateral ureteral obstruction. Without obstruction, kidneys from decorin–/– mice did not differ in any aspect from their WT counterparts. However, already 12 h after obstruction, decorin–/– animals showed lower levels of p27KIP1 and soon thereafter a more pronounced up-regulation and activation of initiator and effector caspases, followed by enhanced apoptosis of tubular epithelial cells. At later stages, a higher increase of TGF-β1 became apparent. After 7 days, there was a 15-fold transient up-regulation of the related proteoglycan biglycan, which was mainly caused by the appearance of biglycan-expressing mononuclear cells. Other small proteoglycans showed no similar response. Owing to enhanced degradation of type-I collagen and increased tubular epithelial cell apoptosis, end-stage kidneys from decorin–/– animals were more atrophic than WT kidneys.Conclusion These data suggest that decorin exerts beneficial effects on renal inflammation, primarily by influencing the expression of a key cyclin-dependent kinase inhibitor, thereby limiting the degree of apoptosis and tubular atrophy. In later stages, anti-fibrotic effects of decorin are based on the regulation of TGF-β1 expression, mononuclear cell infiltration and collagen turnover." @default.
- W1574009689 created "2016-06-24" @default.
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- W1574009689 date "2008-06-28" @default.
- W1574009689 modified "2023-09-26" @default.
- W1574009689 title "Decorin in renal inflammation and fibrosis - more than an inhibitor of TGF-β" @default.
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- W1574009689 doi "https://doi.org/10.1111/j.0959-9673.2004.0369g.x" @default.
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