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Hepatic SATB1 induces paracrine activation of hepatic stellate cells and is upregulated by HBx

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单位: [1]Huazhong Univ Sci & Technol, Tongji Hosp, Dept Gastroenterol, Tongji Med Coll, Wuhan 430030, Peoples R China [2]Huazhong Univ Sci & Technol, Tongji Hosp, Dept Pediat, Tongji Med Coll, Wuhan 430030, Peoples R China
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Chronic hepatitis B virus (HBV) infection is a major cause of chronic liver diseases, but its involvement in hepatic fibrogenesis remains unclear. Special AT-rich binding protein 1 (SATB1) has been implicated in reprogramming chromatin organization and transcription profiles in many cancers and non-cancer-related conditions. We found that hepatic SATB1 expression was significantly up-regulated in fibrotic tissues from chronic hepatitis B virus (HBV)-infected patients and HBV transgenic (HBV-Tg) mouse model. Knockdown of SATB1 in the liver significantly alleviated CCl4-induced fibrosis in HBV-Tg mouse model. Moreover, we suggested HBV encoded x protein (HBx) induced SATB1 expression through activation of JNK and ERK pathways. Enforced expression of SATB1 in hepatocytes promoted the activation and proliferation of hepatic stellate cells (HSCs) by secretion of connective tissue growth factor (CTGF), Interleukin-6 (IL-6) and platelet derived growth factor-A (PDGF-AA). Our findings demonstrated that HBx upregulated hepatic SATB1 which exerted pro-fibrotic effects by paracrine activation of stellate cells in HBV-related fibrosis.

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出版当年[2015]版:
大类 | 2 区 综合性期刊
小类 | 2 区 综合性期刊
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大类 | 3 区 综合性期刊
小类 | 3 区 综合性期刊
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Q1 MULTIDISCIPLINARY SCIENCES
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Q1 MULTIDISCIPLINARY SCIENCES

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第一作者单位: [1]Huazhong Univ Sci & Technol, Tongji Hosp, Dept Gastroenterol, Tongji Med Coll, Wuhan 430030, Peoples R China
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