2014
DOI: 10.1590/1414-431x20143679
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Dynamic expression of desmin, α-SMA and TGF-β1 during hepatic fibrogenesis induced by selective bile duct ligation in young rats

Abstract: We previously described a selective bile duct ligation model to elucidate the process of hepatic fibrogenesis in children with biliary atresia or intrahepatic biliary stenosis. Using this model, we identified changes in the expression of alpha smooth muscle actin (α-SMA) both in the obstructed parenchyma and in the hepatic parenchyma adjacent to the obstruction. However, the expression profiles of desmin and TGF-β1, molecules known to be involved in hepatic fibrogenesis, were unchanged when analyzed by semiqua… Show more

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Cited by 16 publications
(12 citation statements)
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References 29 publications
(48 reference statements)
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“…Two analysis methods, semiquantitative and quantitative PCR, were utilized in the current investigation to provide a better estimation of the results. The expression levels of both genes coincided, in agreement with previous results of investigations performed in our laboratory 12 .…”
Section: Discussionsupporting
confidence: 91%
“…Two analysis methods, semiquantitative and quantitative PCR, were utilized in the current investigation to provide a better estimation of the results. The expression levels of both genes coincided, in agreement with previous results of investigations performed in our laboratory 12 .…”
Section: Discussionsupporting
confidence: 91%
“…21 TGF-β1 is considered as a major profibrogenic cytokine. 22 TGF-β1 regulates a wide variety of cellular processes in liver fibrogenesis, including apoptosis of hepatocytes, enhances hepatocyte destruction, and mediate hepatic stellate cell and fibroblast activation resulting in a wound healing response with extracellular matrix deposition. TGF-β1 also regulates activation and recruitment of inflammatory cells into injured liver, and transdifferentation of some liver-resident cells.…”
Section: Discussionmentioning
confidence: 99%
“…In response to inflammatory response, TGF-β1 drives myofibroblast activation through both canonical (Smad-based) and non-canonical (non-Smad-based) signaling pathways, leading to excessive ECM deposition and resultant fibrosis in synovium (3). Large amounts of TGF-β1 are stored in ECM accumulation; the activation and proliferation of myofibroblast correlate with a high expression of α-smooth muscle actin (α-SMA), which is considered myofibroblast marker (4). Similar to the action in diabetic nephropathy (5), pulmonary fibrosis (6), and liver fibrosis (7), TGF-β1 levels are elevated in the synovial fluid of arthritis patients, correlating with up-regulated genes involved in ECM turnover (8).…”
Section: Introductionmentioning
confidence: 99%