Role of hepatitis B virus in intrahepatic TGF-β1/Smads signaling pathway |
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Authors: | ZHANG Xiang-mei LE Xiao-hua CHEN Pei-fen GOU Ji-zhou SUN Yan ZHONG Xun-zhen ZHOU Ya-min LIU Xiao-ling CHEN Qing-shan |
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Institution: | 1.Department of Pathology, the Third Peoples Hospital of Shenzhen, Shenzhen 518112, China;2.Epidemiology Division, School of Medicine, Jinan University, Guangzhou 510632, China. |
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Abstract: | AIM:To explore the effects of hepatitis B virus (HBV) on intrahepatic expression of transforming growth factor β1(TGF-β1) and Smads. METHODS:The expression of intrahepatic TGF-β1, HBsAg and HBcAg in control group and chronic hepatitis B (CHB) group was detected by immunohistochemical method.The serum HBV DNA content was determined by real-time PCR. The role of HBV in the expression of TGF-β1, Smad3 and Smad7 in human hepatic stellate cell line LX-2 in vitro was observed by cell culture and Western blotting. RESULTS:The average score of intrahepatic TGF-β1 expression in CHB group was higher than that in control group. With the increase in serum HBV DNA content, intrahepatic TGF-β1 expression was also enhanced. In the HBcAg positive hepatic tissue, there was higher TGF-β1 expression than that in the liver tissue of HBcAg negative. Compared with control group and HBV+anti-TGF-β1 group, HBV caused increased expression of TGF-β1 and Smad3 in HBV group in vitro. No difference of Smad7 protein among control group, HBV group and HBV+anti-TGF-β1 group was observed. CONCLUSION: The expression of intrahepatic TGF-β1 is related to serum HBV DNA and hepatocellular HBcAg in the patients with CHB. HBV-induced liver fibrosis mainly relies on positive regulatory mechanisms of Smad3,and the negative regulation by Smad7 almost does not function. |
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Keywords: | Hepatitis B virus Transforming growth factor β1 Smad proteins Liver fibrosis |
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