![]() ![]() Conclusion: OPN has been implicated in fibrosis in several organs. Since senescence-associated β-galactosidase activity was detected in those cells both in vitro and in vivo, these cells probably were terminally differentiated senescent myofibroblasts. Both in vivo and in vitro experiments showed that a novel population of multinucleated α-smooth muscle actin +CD90 – myofibroblast-like cells, which surrounded fibrotic tissue, was the main source of OPN during progression of fibrosis. Immunofluorescence showed that fibrotic tissues in glomeruli accumulated massive deposits of extracellular OPN. Two-dimensional electrophoresis showed that the expressed OPN was in three major isoforms. Results: DNA microarray for ECM genes, quantitative RT-PCR and Western blot revealed significant upregulation of osteopontin (OPN), a multifunctional molecule, in the glomeruli only after onset of glomerular fibrosis. Immunofluorescence was applied to identify cell sources for the molecules. Methods: Expression of ECM genes in glomeruli was determined at RNA and protein levels. We investigated the association between expression of extracellular matrix (ECM) proteins and progression of glomerular fibrosis. In our rat model for anti-glomerular basement membrane GN, severe fibrosis follows glomerular inflammation. Background: Glomerular fibrosis is the common end result of glomerulonephritis (GN) regardless of etiology. ![]()
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