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)

Immunohistochemical methods were used to distinguish idiopathic pulmonary fibrosis (IPF) from interstitial pneumonia associated with rheumatoid arthritis (RA lung). The subjects were six patients with IPF and seven with RA lung, in whom the pathological findings were consistent with usual interstitial pneumonia. Antibodies to vimentin (Vim), alpha-smooth muscle actin (alpha-SMA), and S-100 protein were used for immunohistochemical studies done by the streptavidin-biotin-peroxidase complex method. In fibrosis associated with RA lung, proliferation of both Vim and alpha-SMA-positive myofibroblasts was widely observed, despite pathological findings of honeycombing, usual interstitial pneumonia, and BOOP. Fibrosis in cases of IPF was found to be characterized mainly by Vim-positive fibroblasts, and on occasion was associated with hyperplasia of smooth muscle. Lung tissues from patients with acute exacerbations of RA lung, especially when associated with a BOOP pattern, had many cells positive for S-100 protein. However, such cells were generally hard to find in cases of IPE. Similar results were obtained with regard to the honeycomb pattern in both IPF and RA lung. These findings suggest that IPF and RA lung can be fairly clearly differentiated based on the proliferation of myofibroblasts and on the presence or absence of cells positive for S-100 protein.
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PMID:[Immunohistochemical study of fibrosis and S-100 protein-positive cells in idiopathic pulmonary fibrosis and in interstitial pneumonia associated with rheumatoid arthritis]. 871 85

The aim of the investigation was to study the specific features of morphological manifestations and the molecular bases of lung tissue remodeling in progressive idiopathic pulmonary fibrosis (IPF). The investigation used open and transbronchial biopsy specimens from 110 patients with IPE/idiopathic pneumonia syndrome in 1997 to 2008. Immunohistochemical analysis was carried out on serial paraffin-embedded lung tissue slices from 20 patients with IPF and 20 control patients. Immunohistochemical staining for the detection of antigens in the paraffin-embedded slices was made using the antibodies to MMP-1, MMP-2, MMP-7, TIMP-4, Apo-CAS, PCNA, PDGF, EGFR, CD34, and SMA. Nonparametric statistical methods were employed. Our findings have indicated that in early-stage IPF, there are proliferating myofibroblasts in the myofibroblastic foci, mainly in the bronchioloalveolar transitional zone (BATZ), which express PCNA and PDGF. Both in early- and late-stage IPF, there were signs of increased readiness of the alveolar and bronchiolar epithelium of BATZ for apoptosis, as judged from Apo-CAS expression. At the same time no Apo-CAS expression was recorded in the myofibroblasts. In the early stage of the disease, the expression of MMP-1, MMP-2, MMP-7, and TIMP-4 in the epitheliocytes, macrophages, fibroblasts, and myofibroblasts was higher than that in the late stage of IPF. At the same time, late-stage IPF was characterized by the higher expression in all lung tissue cells than was early-stage IPF. There was also a significant increase in vessel density in both early and late stages of IPF as compared with intact lung tissue particularly in the BATZ in the control group. Thus, lung tissue remodeling in the progression of IPF from the early to late stage of the disease comprises interrelated processes that are largely localized in the BATZ, such as immune inflammation with pathological reparation, neoangiogenesis, apoptosis, and proliferation of epitheliocytes and myofibroblasts, which lead to the development of interstitial fibrosis and adenomatosis of the lung.
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PMID:[The mechanism of lung tissue remodeling in the progression of idiopathic pulmonary fibrosis]. 2108 35