Liver international : official journal of the International Association for the Study of the Liver · 2004
Hypoxia potentiates transforming growth factor-beta expression of hepatocyte during the cirrhotic condition in rat liver.
Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Jeong Won-Ii, Do Sun-Hee, Yun Hae-Sun, Song Byoung-Joon, Kim Seong-Jin, Kwak Wie-Jong, Yoo Sung-Eun, Park Ho-Yong, Jeong Kyu-Shik
Аннотация
BACKGROUND/AIMS: Many studies have reported that hypoxia might be associated with angiogenesis and fibrogenesis, and the level of transforming growth factor-beta1 (TGF-beta1) was increased in fibrotic liver and maximal at cirrhosis. Therefore, we examined the expression of TGF-beta1, phosphorylated-Smad2/3 (p-Smad2/3) of the TGF-beta immediate down stream signaling system and hypoxic status during hepatic fibrogenesis.
METHODS: Fibrosis of rats was induced by carbon tetrachloride. Collagens were detected with Azan stain. Immunohistochemistry and immunoblotting was used.
RESULTS: TGF-beta1 was mainly produced by hypoxic hepatocytes at cirrhosis although myofibroblasts (MFBs) and macrophages producing TGF-beta1 were decreased. Moreover, distribution of p-Smad2/3 in hepatocytes was consistent with those of hypoxic hepatocytes regardless of MFBs. Furthermore, in recovery, most MFBs disappeared, whereas positive reactions of p-Smad2/3 still existed in the hepatocytes of hypoxic areas. Therefore, TGF-beta1 expression in hepatocytes might have been associated with hypoxia.
CONCLUSIONS: We put forward the hypothesis that TGF-beta1 is mainly produced by MFBs and macrophages at early and middle stages of fibrotic processes, but it is predominantly released by hypoxic hepatocytes in the last fibrotic stage or cirrhosis.
METHODS: Fibrosis of rats was induced by carbon tetrachloride. Collagens were detected with Azan stain. Immunohistochemistry and immunoblotting was used.
RESULTS: TGF-beta1 was mainly produced by hypoxic hepatocytes at cirrhosis although myofibroblasts (MFBs) and macrophages producing TGF-beta1 were decreased. Moreover, distribution of p-Smad2/3 in hepatocytes was consistent with those of hypoxic hepatocytes regardless of MFBs. Furthermore, in recovery, most MFBs disappeared, whereas positive reactions of p-Smad2/3 still existed in the hepatocytes of hypoxic areas. Therefore, TGF-beta1 expression in hepatocytes might have been associated with hypoxia.
CONCLUSIONS: We put forward the hypothesis that TGF-beta1 is mainly produced by MFBs and macrophages at early and middle stages of fibrotic processes, but it is predominantly released by hypoxic hepatocytes in the last fibrotic stage or cirrhosis.
Предметные рубрики MeSH
AnimalsCarbon TetrachlorideCells, CulturedCollagenDNA-Binding ProteinsHepatocytesHypoxiaImmunoblottingImmunohistochemistryLiver Cirrhosis, ExperimentalMaleProbabilityRNA, MessengerRatsRats, WistarReceptors, Transforming Growth Factor betaReference ValuesSensitivity and SpecificitySmad2 ProteinSmad3 ProteinTrans-Activators