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Animal Model |
From the Departments of Internal Medicine D,*
Physiological Chemistry and Pathobiochemistry,
and Arteriosclerosis Research,¶
University ofMünster, Münster, Germany; the Department of Cellular andMolecular Pathology,
German Cancer ResearchCenter, Heidelberg, Germany; the Department of Pathology, Anatomy, andCell Biology,||
Thomas Jefferson University, Philadelphia,Pennsylvania; and the Institute of MolecularBiology,
Slovak Academy of Sciences,Bratislava, Slovak Republic
Decorin, a small dermatan-sulfate proteoglycan, participates in extracellular matrix assembly and influences directly and indirectly cell behavior via interactions with signaling membrane receptors and transforming growth factor (TGF)-ß. We have therefore compared the development of tubulointerstitial kidney fibrosis in wild-type (WT) and decorin-/- mice in the model of unilateral ureteral obstruction. Without obstruction, kidneys from decorin-/- mice did not differ in any aspect from their WT counterparts. However, already 12 hours 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. Later, a higher increase of TGF-ß1 became apparent. After 7 days, there was an up to 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. Because of enhanced degradation of type I collagen, end-stage kidneys from decorin-/- animals were more atrophic than WT kidneys. These data suggest that decorin exerts beneficial effects on tubulointerstitial fibrosis, primarily by influencing the expression of a key cyclin-dependent kinase inhibitor and by limiting the degree of apoptosis, mononuclear cell infiltration, tubular atrophy, and expression of TGF-ß1.
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