2002
DOI: 10.1053/jhep.2002.30083
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Differential regulation of TGF-β signal in hepatic stellate cells between acute and chronic rat liver injury

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Cited by 173 publications
(131 citation statements)
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“…For example, tumor necrosis factor-α (TNF-α)-induced abrogation of TGF-β-dependent profibrotic responses was linked to the induction of endogenous Smad7 (20). On the other hand, defective Smad7 induction is implicated in the exaggerated TGF-β responsiveness characteristic of hepatic cells and myofibroblasts from chronically injured livers (21,22). In the present study, we observed that the expression of Smad7 began to increase after TGF-β treatment for 4 h. These data agree well with previous results obtained for skin fibroblasts (23).…”
Section: Discussionsupporting
confidence: 93%
“…For example, tumor necrosis factor-α (TNF-α)-induced abrogation of TGF-β-dependent profibrotic responses was linked to the induction of endogenous Smad7 (20). On the other hand, defective Smad7 induction is implicated in the exaggerated TGF-β responsiveness characteristic of hepatic cells and myofibroblasts from chronically injured livers (21,22). In the present study, we observed that the expression of Smad7 began to increase after TGF-β treatment for 4 h. These data agree well with previous results obtained for skin fibroblasts (23).…”
Section: Discussionsupporting
confidence: 93%
“…TGF-b has been shown to be a key profibrogenic cytokine, as it has a prominent role in the production of extracellular matrix by activated HSC. 29 In particular, TGF-b1, which is a well-studied mediator in hepatic fibrogenesis, promotes HSC transition into the myofibroblast 29 and is involved in the formation of a-SMA fiber formation in the myofibroblast. 30 The major cellular mechanisms of CCl 4 are suggested to produce free radicals, which damage the hepatocyte by causing lipid peroxidation and binding cell structures.…”
Section: Discussionmentioning
confidence: 99%
“…Aberrant regulation of Smad7 activity could be implicated in the development of human diseases, such as inflammatory bowel diseases and scleroderma, in which inappropriate expression of TGF-␤ has been shown to play, at least in part, a causative role (5,6). In chronic rat liver injury, the constitutive phosphorylation of Smad2 under a low level of Smad7 could be involved in the progression of liver fibrosis, whereas a transient induction of Smad7 terminated Smad2 phosphorylation in acute liver injury (19). However, controversy concerning the levels of Smad7 in kidney diseases remains; Uchida et al (20) reported a decrease in glomerular expression of Smad7 in anti-Thy-1 nephritis, which is an experimental model of acute reversible mesangial proliferative glomerulonephritis in rats.…”
Section: Discussionmentioning
confidence: 99%