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Use of prostaglandin I2 analog in treatment of massive hepatic necrosis associated with endothelial cell injury and diffuse sinusoidal fibrin deposition (1995)

Fujiward, Kenji ; Mochida, Satoshi ; Ohno, Akihiko ; [et al.]

Springer

Digestive diseases and sciences 40 (1995), S. 41-47

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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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Rat liver fat-storing cell lines express sarcomeric myosin heavy chain mRNA and protein (1993)

Ogata, Itsuro ; Sáez, Claudia G. ; Greenwel, Patricia ; [et al.]

New York, NY : Wiley-Blackwell

Cell Motility and the Cytoskeleton 26 (1993), S. 125-132

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ISSN: 0886-1544

Keywords: lipocytes ; liver cirrhosis ; myofibroblasts ; myosin gene ; Life and Medical Sciences ; Cell & Developmental Biology

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology , Medicine

Notes: Fat-storing cells (FSC, lipocytes, or Ito cells) of liver store vitamin A and are the main producers of extracellular matrix in normal and cirrhotic liver. During liver injury, FSC undergo an activation process characterized by a decrease in vitamin A storage and an increase in cell proliferation and extracellular matrix deposition. This activation process also occurs upon culturing FSC from normal liver. In contrast to most cells of nonmuscle origin, activated FSC express two cytoskeletal proteins normally found in muscle, desmin, and smooth muscle α-actin. Based on their strategic perisinusoidal location, it has been hypothesized that FSC play a role in regulating blood flow. However, the nature of the contractile elements involved in this process remains to be determined. In this communication we demonstrate the presence of a sarcomeric myosin in proteins solubilized from liver biomatrix. In addition we demonstrate the expression of sarcomeric myosin heavy chain (MHC) mRNA and protein in two FSC clones derived from a CCl4-cirrhotic rat liver (CFSC). Through cloning the cDNA corresponding to the MHC gene expressed in these cells we demonstrate that it encodes fast IId skeletal MHC and thus represents a marker normally seen in adult muscle. The unexpected expression of an adult stage skeletal muscle molecular motor in FSC from cirrhotic liver is consistent with the proposed specialized contractile capacity of these cells. © 1993 Wiley-Liss, Inc.

Additional Material: 5 Ill.