title: MicroRNA-155 deficiency attenuates ischemia-reperfusion injury after liver transplantation in mice.
abstract: Liver ischemia-reperfusion injury (IRI) is a major cause of morbidity and mortality after resection surgery, liver transplantation, and hemorrhagic and septic shock. Mir-155 is upregulated by a broad range of inflammatory mediators, and it has been demonstrated to be involved in both innate and adaptive immune responses. However, the role of mir-155 in liver IRI has never been investigated. In this study, mir-155 deficiency protected mice from liver IRI, as shown by lower serum alanine aminotransferase (ALT) levels and Suzuki scores. Mir-155 deficiency results in the development of M2 macrophages, which respond to IR-induced innate immune stimulation by producing a regulatory inflammatory response with higher level of IL-10, but lower levels of TNF-α, IL-6, and IL-12p40. Mir-155 deficiency suppresses IL-17 expression, which contributes to the liver IRI development. In our further in vitro study, the results show that the Th17 differentiation is inhibited by SOCS1 overexpression and the promoted M2 macrophage development induced by mir-155 deficiency is abolished by SOCS1 knockdown. In conclusion, mir-155 deficiency attenuates liver IRI through upregulation of SOCS1, and this was associated with promoted M2 macrophage and inhibited Th17 differentiation.
authors.affiliation: Laboratory of Liver Injury and Repair Molecular Medicine, Guilin Medical University, Guilin, Guangxi, China.|Department of Hepatobiliary Surgery, Guilin Medical University, Affiliated Hospital, Guilin, Guangxi, China.
authors.forename: Bo
authors.initials: B
authors.lastname: Tang
authors.affiliation: Laboratory of Liver Injury and Repair Molecular Medicine, Guilin Medical University, Guilin, Guangxi, China.|Department of Gastrointestinal Surgery, Guilin Medical University, Affiliated Hospital, Guilin, Guangxi, China.
authors.forename: Zhenran
authors.initials: Z
authors.lastname: Wang
authors.affiliation: Department of Pathology and Physiopathology, Guilin Medical University, Guilin, Guangxi, China.
authors.forename: Guangying
authors.initials: G
authors.lastname: Qi
authors.affiliation: Laboratory of Liver Injury and Repair Molecular Medicine, Guilin Medical University, Guilin, Guangxi, China.|Department of Hepatobiliary Surgery, Guilin Medical University, Affiliated Hospital, Guilin, Guangxi, China.
authors.forename: Shengguang
authors.initials: S
authors.lastname: Yuan
authors.affiliation: Laboratory of Liver Injury and Repair Molecular Medicine, Guilin Medical University, Guilin, Guangxi, China.|Department of Hepatobiliary Surgery, Guilin Medical University, Affiliated Hospital, Guilin, Guangxi, China.
authors.forename: Shuiping
authors.initials: S
authors.lastname: Yu
authors.affiliation: Laboratory of Liver Injury and Repair Molecular Medicine, Guilin Medical University, Guilin, Guangxi, China.|Department of Hepatobiliary Surgery, Guilin Medical University, Affiliated Hospital, Guilin, Guangxi, China.
authors.forename: Bo
authors.initials: B
authors.lastname: Li
authors.affiliation: Laboratory of Liver Injury and Repair Molecular Medicine, Guilin Medical University, Guilin, Guangxi, China.|Department of Hepatobiliary Surgery, Guilin Medical University, Affiliated Hospital, Guilin, Guangxi, China.
authors.forename: Yangchao
authors.initials: Y
authors.lastname: Wei
authors.affiliation: Laboratory of Liver Injury and Repair Molecular Medicine, Guilin Medical University, Guilin, Guangxi, China.|Department of Hepatobiliary Surgery, Guilin Medical University, Affiliated Hospital, Guilin, Guangxi, China.
authors.forename: Qi
authors.initials: Q
authors.lastname: Huang
authors.affiliation: Laboratory of Liver Injury and Repair Molecular Medicine, Guilin Medical University, Guilin, Guangxi, China.|Department of Hepatobiliary Surgery, Guilin Medical University, Affiliated Hospital, Guilin, Guangxi, China.
authors.forename: Run
authors.initials: R
authors.lastname: Zhai
authors.affiliation: Laboratory of Liver Injury and Repair Molecular Medicine, Guilin Medical University, Guilin, Guangxi, China.|Department of Hepatobiliary Surgery, Guilin Medical University, Affiliated Hospital, Guilin, Guangxi, China.
authors.forename: Songqing
authors.initials: S
authors.lastname: He
mesh_terms: D056704:Adaptive Immunity; D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology; D002454:Cell Differentiation; D002469:Cell Separation; D004195:Disease Models, Animal; D005434:Flow Cytometry; D007113:Immunity, Innate; D007249:Inflammation; D016753:Interleukin-10 / Q000378:metabolism; D053762:Interleukin-12 Subunit p40 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D007728:Kupffer Cells / Q000166:cytology; D008099:Liver / Q000378:metabolism; D016031:Liver Transplantation; D008264:Macrophages / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D035683:MicroRNAs / Q000235:genetics* / Q000502:physiology; D009195:Peroxidase / Q000378:metabolism; D015427:Reperfusion Injury / Q000276:immunology*; D000071222:Suppressor of Cytokine Signaling 1 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000235:genetics; D058504:Th17 Cells / Q000166:cytology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D015854:Up-Regulation
chemical_list: C556062:IL10 protein, mouse; D053762:Interleukin-12 Subunit p40; D015850:Interleukin-6; D035683:MicroRNAs; C532623:Mirn155 microRNA, mouse; C491590:Socs1 protein, mouse; D000071222:Suppressor of Cytokine Signaling 1 Protein; D050826:Suppressor of Cytokine Signaling Proteins; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D009195:Peroxidase; D000410:Alanine Transaminase
keywords: M2 macrophage; Mir-155; SOCS1; Th17; liver IRI