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  • 1
    Electronic Resource
    Electronic Resource
    Increased expression of osteopontin in activated Kupffer cells and hepatic macrophages during macrophage migration in Propionibacterium acnes-treated rat liver (2000)
    Springer
    Journal of gastroenterology 35 (2000), S. 696-701 
    Details
    ISSN: 1435-5922
    Keywords: Key words: osteopontin ; hepatic macrophages ; Kupffer cells ; MCP-1 ; MIP-1α ; Propionibacterium acnes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract: Osteopontin is an extracellular matrix component that can act as a chemokine to induce macrophage migration. The significance of osteopontin in macrophage infiltration into the liver was examined in rats given heat-killed Propionibacterium acnes. In normal rats, osteopontin mRNA expression in the liver was mini-mal, determined by quantitative-competitive reverse transcription-polymerase chain reaction (RT-PCR) assay. Northern blot analysis revealed that osteopontin mRNA was not expressed in Kupffer cells isolated from normal rats. When rats received heat-killed P. acnes intravenously, marked macrophage accumulation, forming granulomas, developed in the liver later than 3 days after the injection and its extent became maximal between 5 and 7 days. In these rats, osteopontin mRNA expression was increased in the liver later than 1 day (with its peak at 3 days after the injection), and the mRNA expression was increased markedly in Kupffer cells and hepatic macrophages isolated at 7 days. The mRNA expression of monocyte chemotactic protein-1 (MCP-1) and macrophage inflammatory protein-1α (MIP-1α), chemokines for monocytes and macrophages, was also increased in the liver of P. acnes-treated rats, with peak expression at 3 days. We conclude that osteopontin derived from Kupffer cells and hepatic macrophages may contribute to the infiltration of monocytes and macrophages into the liver cooperatively with the actions of MCP-1 and MIP-1α in P. acnes-treated rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s005350070049
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  • 2
    Electronic Resource
    Electronic Resource
    Use of prostaglandin I2 analog in treatment of massive hepatic necrosis associated with endothelial cell injury and diffuse sinusoidal fibrin deposition (1995)
    Springer
    Digestive diseases and sciences 40 (1995), S. 41-47 
    Details
    ISSN: 1573-2568
    Keywords: Prostaglandin I2 ; beraprost sodium ; hepatic necrosis ; intravascular coagulation ; sinusoidal endothelial cells ; cytoprotection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Endothelial cell damage causes massive hepatic necrosis as a result of fibrin deposition in the hepatic sinusoids. When a stable analog of prostaglandin I2, beraprost sodium, was administered to rats given either dimethylnitrosamine, carbon tetrachloride, or endotoxin followingCorynebacterium parvum administration, the hepatic necrosis produced in each was attenuated, but to a greater extent in the dimethylnitrosamine and endotoxin/Corynebacterium parvum models, where fibrin deposition in the hepatic sinusoids occurs, as compared to the carbon tetrachloride model, where such fibrin deposition does not occur. Beraprost sodium reduced the expected increase of portal venous pressure in the endotoxin/Corynebacterium parvum model without affecting plasma thrombin-antithrombin III complex levels. Beraprost sodium also significantly reduced cell killing of both isolated rat hepatocytes and hepatic sinusoidal endothelial cells exposed totert-butyl hydroperoxide when compared to controls. Beraprost sodium could prove to be a therapeutic candidate for the treatment of hepatic necrosis, particularly in cases associated with fibrin deposition in the hepatic sinusoids because of its fibrin clot-clearning action.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02063939
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  • 3
    Electronic Resource
    Electronic Resource
    Fat-storing cell abnormalities associated with endothelial cell damage after cold ischemic storage of rat liver in UW solution (1994)
    Springer
    Digestive diseases and sciences 39 (1994), S. 861-865 
    Details
    ISSN: 1573-2568
    Keywords: fat-storing cell ; sinusoidal endothelial cell ; cold ischemic storage ; University of Wisconsin solution
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Rat liver was stored at 1° C in University of Wisconsin solution, and morphological changes were observed after 12, 18, 24, and 36 hr by transmission electron microscopy. There were two types of endothelial cell damage in the hepatic sinusoids. One was disruption of the endothelial linings, and the other detachment of endothelial cells into the sinusoidal space accompanied by fat-storing cell abnormalities. The former damage was seen after storage longer than 12 hr, while the latter developed after 18 hr even in the hepatic sinusoids with no disruption of the linings. Considering that fat-storing cell damage can produce endothelial cell destruction, this damage should be given attention as one of factors of endothelial cell destruction in the hepatic sinusoids after cold storage of the liver.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02087434
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    Paper (German National Licenses)
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