Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

IgA nephropathy is generally considered to be an immune-complex-mediated or aggregated (polymerized) IgA (IgA1)-mediated glomerulonephritis. Since the pathogenesis of IgA nephropathy is still obscure, it is important to determine the initiation and progression of this disease using the spontaneous animal model. The ddY mouse strain can serve as a spontaneous animal model for IgA nephropathy. Genetic factors are considered to be involved in the initiation and progression of IgA nephropathy. It has been hypothesized that susceptibility genes for IgA nephropathy can be detected by a genome-wide scan using this model. The peak marker D10MIT 86 on chromosome 10 is located on the region syntenic to human 6q22-23 with IGAN1, which is responsible for familiar IgA nephropathy. There are several developmental and/or exacerbating factors in this disease. Among them, the loss of glomerular epithelial cells (podocytes) and interstitial mast cell infiltration are important factors for progression of glomerulosclerosis and tubulointerstitial injury in patients with IgA nephropathy.
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PMID:Pathogenesis of IgA nephropathy. 1749 30

IgA nephropathy (IgAN) is a kidney disease with a varying renal prognosis. Recently, many studies have demonstrated that renal alpha-smooth muscle actin (alpha-SMA) and transforming growth factor (TGF-beta1) expression, as well interstitial mast cell infiltrates could represent a prognostic marker in several renal diseases. The aim of our study was to analyze the prognostic value of mast cell, TGF-beta1 and alpha-SMA expression in IgAN. A survey of the medical records and renal biopsy reports of 62 patients with a diagnosis of IgAN followed-up from 1987 to 2003 was performed. The mean follow-up time was 74.7 +/- 50.0 months. The immunohistochemical studies were performed using a monoclonal antibody anti-human mast cell tryptase, a polyclonal antibody anti-human TGF-beta1, and a monoclonal antibody anti-human alpha-SMA. An unfavorable clinical course of IgAN was related to interstitial mast cell infiltrates and alpha-SMA expression in the tubulointerstitial area. Expression of glomerular TGF-beta1 and alpha-SMA, and interstitial TGF-beta1 is not correlated with clinical course in IgAN. In conclusion, the increased number of mast cells and higher alpha-SMA expression in the tubulointerstitial area may be predictive factors for the poor prognosis of patients with IgAN.
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PMID:Mast cells, TGF-beta1 and alpha-SMA expression in IgA nephropathy. 1833 40