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 453 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Multiple injections of D-galactosamine induce liver fibrosis and cirrhosis in rats. The purpose of this immunopathological study was to correlate inflammation and hepatic extracellular matrix remodeling after repeated administration of galactosamine. Rats were given 10, 20, 30, 40, 60, 80, 100 and 140 intraperitoneal injections of D-galactosamine (500 mg/kg body wt, three times weekly). Controls received injections of saline solution. Cryostat sections of liver tissue obtained on biopsy or autopsy were immunostained with a panel of monoclonal and polyclonal monospecific antibodies reactive with macrophages, T and B lymphocytes, desmin, the extracellular matrix components fibronectin; laminin; collagen types I, III and IV; and the fibronectin receptor alpha 5 beta 1. Total RNA was extracted and Northern-blot analysis was performed with a specific cDNA probe for rat collagen type III. Spotty liver cell necrosis and mild portal and parenchymal inflammation was seen after 10 injections of galactosamine. After 20 to 40 injections, expansion of protal tracts, prominent bile ductular proliferation and gradual formation of fibrous septa were encountered with the development of cirrhosis at later intervals. These progressive histological changes were paralleled by a gradual increase of desmin-positive cells in developing septa with deposition of fibronectin; collagen types I, III, and IV; and laminin. Northern-blot analysis showed that this accumulation of extracellular matrix was not accompanied by increase of mRNA for collagen type III. In conclusion, repetitive administration of galactosamine causes progressive liver disease with prominent bile ductule proliferation and development of fibrous septa. These pathological alterations bear some resemblance to the morphological changes in chronic biliary disease in human beings.
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PMID:Immunohistochemical study of hepatic fibrosis induced in rats by multiple galactosamine injections. 750 72

Stress fibers (SFs) are present along the apical (apical SF) and the basal (basal SF) portions of cultured cells. We have recently shown that apical SFs are anchored to the apical plasma membrane (PM) in a manner similar to how basal SFs are attached to focal adhesion sites. We propose calling such apical SF-membrane attachment sites "apical plaques." To study the macromolecular composition of the apical plaque and the focal adhesion in endothelial cells (ECs) in situ, we examined by confocal laser scanning and fluorescence microscopy guinea pig aortae stained with various antibodies against focal adhesion-associated proteins. Basal SFs oriented parallel to the blood flow direction were mainly located in the upstream half of the cell. Thin apical SFs were also observed. Spotty staining patterns were observed in the basal and the apical portions of cells stained with anti-vinculin, anti-talin, anti-paxillin, or anti-fibronectin receptor, indicating the presence of focal adhesions and apical plaques in ECs in situ. Although fibronectin receptors were present in the apical plaque, fibronectin was not detected on the apical cell surface. Our data suggest that the molecules responsible for the SF-PM association are the same between in vitro and in situ cells. Our results appear to support a hypothesis that the SF system is involved in sensing and/or signal transduction of fluid mechanical forces.
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PMID:Macromolecular composition of stress fiber-plasma membrane attachment sites in endothelial cells in situ. 888 92