Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q16637 (SMA)
8,107 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although most studies suggest that the hypercellularity in mesangial proliferative nephritis is due to increased cell proliferation, we hypothesized that it may also be due to increased expression of survival factors that may block their removal (apoptosis). We therefore studied the expression of apoptosis preventing/delaying the bcl-2 gene product in the glomerulus with various human glomerulonephritides. Immunohistochemistry for Bcl-2, proliferating cell associated protein (Ki-67) and alpha-smooth muscle actin (alpha-SMA) was performed on 55 biopsied kidney tissues: 6 cases of orthostatic proteinuria as a control (OP); 6 cases of diffuse proliferative lupus nephritis (WHO type IV, LN-MPGN); 24 cases of IgA nephropathy (IgA); 9 cases of minimal change nephrosis and 10 cases of idiopathic membranous nephropathy. The number of Ki-67-positive cells and the expression of alpha-SMA in the glomerulus were significantly higher in LN-MPGN and IgA. There was a significant positive correlation between glomerular Bcl-2 expression and glomerular cell proliferation evaluated by the number of Ki-67-positive cells (r=0.605, p < 0.01) or glomerular alpha-SMA expression (r=0.674, p < 0.01). Glomerular expression of Bcl-2 in IgA or LN-MPGN was significantly higher than that in OP (p < 0.01 and p < 0.05 vs. OP, respectively). The Bcl-2-positive cells were present in mesangial locations and demonstrated a perinuclear pattern. These results suggest that maintenance of glomerular hypercellularity in human glomerular diseases is partly due to the prevention of mesangial cell death via Bcl-2 expression.
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PMID:Mesangial proliferative nephritis in man is associated with increased expression of the cell survival factor, Bcl-2. 965 32

Fourteen renal biopsy specimens from patients with mesangiocapillary glomerulonephritis type I (MCGN-I), for whom both light and electron microscopies as well as immunofluorescence microscopy and full clinical data were available, were examined quantitatively. As a control, 10 biopsy specimens of the kidney from patients with minimal change disease (MCD) were used. Morphometric investigations were performed by a computer image analysis system to investigate whether myofibroblasts have a role in tubulointerstitial fibrosis in MCGN-I and, in particular, to examine the relationship between alpha-SMA expression and interstitial infiltrates. The morphometric study revealed that in MCGN-I patients the mean values for the expression of alpha-SMA, interstitial volume, CD68+, CD45RB+, CD43+ and CD20+ cells were significantly increased, as compared with a control group. In the MCGN-I group, there were significant positive correlations between the interstitial expression of alpha-SMA and the interstitial volume as well as CD68+ and CD45RB+ cells. The correlations between the interstitial expression of alpha-SMA and CD43+ as well as CD20+ cells were positive, but without statistical significance. In conclusion, our study suggests that interstitial a-SMA positive cells play a role in the development of interstitial fibrosis in MCGN-I. The significant correlation between the interstitial expression of alpha-SMA and interstitial CD68+ cells may identify monocytes/macrophages as important mediators in the process of inducing the myofibroblast phenotype in resting fibroblasts.
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PMID:Quantitative analysis of the interstitial myofibroblasts in idiopathic mesangiocapillary glomerulonephritis type I. 1054 29

Fourteen renal biopsy specimens from patients with mesangiocapillary glomerulonephritis type I (MCGN-I) for whom both light and electron microscopy as well as immunofluorescence microscopy and full clinical data were available were examined quantitatively. As a control 10 biopsy specimens of kidneys removed because of trauma were used. Morphometric investigations were performed by means of a computer image analysis system to evaluate whether mast cells have a role in tubulointerstitial fibrosis in MCGN-I and to examine the relationship between mast cells and interstitial alpha-smooth muscle actin (alpha-SMA) expression as well as interstitial infiltrates. The morphometric study revealed that the mean values of the interstitial tryptase positive cells, expression of alpha-SMA, interstitial volume, CD 68+, CD 45RB+, CD 43+ and CD 20+ cells were significantly increased in MCGN-I patients in comparison with control group. In MCGN-I group there were significant positive correlations between interstitial tryptase positive cells and interstitial expression of alpha-SMA, interstitial volume, serum creatinine as well as CD 43+ and CD 68+ cells. The correlations between interstitial tryptase positive cells and CD 45+, as well as CD 20+ cells did not reach statistical significance. In conclusion, our findings demonstrate that mast cells are one of the constitutive cell types in the interstitium in MCGN-I. Additionally, significant positive correlations between interstitial mast cell count and relative interstitial volume as well as serum creatinine concentration suggest the role of these cells in the development of interstitial fibrosis which may contribute to the renal deterioration in patients with MCGN-I.
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PMID:Quantitative analysis of the interstitial mast cells in idiopathic mesangiocapillary glomerulonephritis type I. 1147 6