title: Stellate Cell Activation and Imbalanced Expression of TGF-β1/TGF-β3 in Acute Autoimmune Liver Lesions Induced by ConA in Mice.
abstract: Objective. To study the pathogenic feature of liver injury, activation of hepatic stellate cells, and dynamic expression of TGF-β1/TGF-β3 to reveal their role in liver injury induced by ConA.Methods. Mice were randomly divided into control group and ConA treatment group. ConA (20 mg/kg) was injected through vena caudalis in ConA treatment group; the controls received the same volume of saline injection. After injection for 2 h, 8 h, 24 h, and 48 h, animals were terminated. Blood, liver, and spleen were harvested. Liver function and histopathology were studied.α-SMA, vimentin, TGF-β1, and TGF-β3 were detected.Results. After ConA injection, liver damage started to increase. Expression ofα-SMA, vimentin, TGF-β1, and TGF-β3 was significantly enhanced; all above indicators reached peak at 8 h; but from 24 h after ConA injection, TGF-β3 expression began to decline, while the TGF-β1/TGF-β3 ratio at 48 h was significantly lower than control.Conclusion. (1) Autoimmune liver injury induced by ConA showed time-based features, in which the most serious liver lesions happened at 8 h after ConA injection. (2) Early activation of HSC and imbalance expression of TGF-β1 and TGF-β3 existed in ConA-induced acute autoimmune liver injury, which may be associated with liver dysfunction and the mechanisms of progression to fibrosis.
authors.affiliation: Division of Gastroenterology, Shandong Provincial Qianfoshan Hospital, Jinan, Shandong, China; Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
authors.forename: Liyun
authors.identifier: 0000-0003-1221-7955
authors.initials: L
authors.lastname: Wang
authors.affiliation: Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
authors.forename: Lei
authors.initials: L
authors.lastname: Tu
authors.affiliation: Division of Neurology, Shandong Provincial Qianfoshan Hospital, Jinan, Shandong, China.
authors.forename: Jinping
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
authors.forename: Keshu
authors.identifier: 0000-0003-3979-4840
authors.initials: K
authors.lastname: Xu
authors.affiliation: Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Qian
mesh_terms: D000208:Acute Disease; D000818:Animals; D001327:Autoimmune Diseases / Q000097:blood / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D015415:Biomarkers / Q000378:metabolism; D003208:Concanavalin A; D005260:Female; D055166:Hepatic Stellate Cells / Q000378:metabolism* / Q000473:pathology*; D007150:Immunohistochemistry; D007275:Injections, Intravenous; D008099:Liver / Q000201:enzymology / Q000473:pathology* / Q000503:physiopathology; D008111:Liver Function Tests; D051379:Mice; D013154:Spleen / Q000473:pathology; D013997:Time Factors; D000637:Transaminases / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000097:blood / Q000378:metabolism*; D053782:Transforming Growth Factor beta3 / Q000097:blood / Q000378:metabolism*; D014746:Vimentin / Q000378:metabolism
chemical_list: D015415:Biomarkers; D053773:Transforming Growth Factor beta1; D053782:Transforming Growth Factor beta3; D014746:Vimentin; D003208:Concanavalin A; D000637:Transaminases