title: [Exogenous HBx promotes epithelial-mesenchymal transition of hepatic progenitor cells in Kunming mice].
abstract: Objective To construct an animal model in which hepatitis B virus X protein (HBx) directly affect hepatic progenitor cells (HPCs), and investigate the potential mechanisms underlying epithelial-mesenchymal transition (EMT) of HPCs. Methods Kunming mice were given 2 mL/L carbon tetrachloride (CCL4) in oil solution by gavage twice a week. Four weeks later, HPCs transfected with recombinant lentiviral vectors stably expressing HBx gene as well as empty vectors were separately injected into the mice via the portal vein, and at the same time, the mice underwent a partial hepatectomy. The gavage twice a week continued after the operation. And on days 3, 5, 7, 14, 21 28 postoperation, the mice were sacrificed and the livers were removed. Fluorescence quantitative PCR was used to detect the mRNA expression level of HBx; immunohistochemistry was performed to observe the exogenous cell survival in vivo. The expression levels of E-cadherin, N-cadherin, vimentin and CK18 were assessed by fluorescence quantitative PCR and Western blotting. Results Immunohistochemistry showed that the exogenous cells obviously survived in vivo in the postoperative liver tissues. Moreover, the expression of HBx was enhanced and expanded over time. Fluorescence quantitative PCR and Western blotting showed that overexpressed HBx downregulated the expressions of E-cadherin and CK18, while upregulated the expressions of N-cadherin and vimentin. Conclusion HBx plays an important role in the regulation of EMT of HPCs in vivo.
authors.affiliation: Department of Pathophysiology, Research Center of Molecular Medicine and Cancer, Chongqing Medical University, Chongqing 400016, China.
authors.forename: Xi
authors.initials: X
authors.lastname: Chen
authors.affiliation: Department of Pathophysiology, Research Center of Molecular Medicine and Cancer, Chongqing Medical University, Chongqing 400016, China.
authors.forename: Ting
authors.initials: T
authors.lastname: Wang
authors.affiliation: Department of Pathophysiology, Research Center of Molecular Medicine and Cancer, Chongqing Medical University, Chongqing 400016, China.
authors.forename: Junxiong
authors.initials: J
authors.lastname: Cheng
authors.affiliation: Department of Pathophysiology, Research Center of Molecular Medicine and Cancer, Chongqing Medical University, Chongqing 400016, China. *Corresponding author, E-mail: e738741@126.com.
authors.forename: Jiayi
authors.initials: J
authors.lastname: Huang
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D058750:Epithelial-Mesenchymal Transition; D006509:Hepatitis B / Q000503:physiopathology* / Q000821:virology; D006515:Hepatitis B virus / Q000235:genetics / Q000378:metabolism*; D022781:Hepatocytes / Q000166:cytology* / Q000821:virology*; D006801:Humans; D008099:Liver / Q000166:cytology / Q000821:virology*; D051379:Mice; D013234:Stem Cells / Q000166:cytology / Q000821:virology; D015534:Trans-Activators / Q000235:genetics / Q000378:metabolism*; D054334:Viral Regulatory and Accessory Proteins
chemical_list: D015534:Trans-Activators; D054334:Viral Regulatory and Accessory Proteins; C057628:hepatitis B virus X protein