title: IL-22 is involved in liver regeneration after hepatectomy.
abstract: Hepatocyte proliferation following partial hepatectomy is an important component of liver regeneration, and recent in vitro studies have shown that IL-22 is involved in cellular proliferation in a variety of cell types, including hepatocytes. IL-22 functions through IL-10Rbeta and IL-22Ralpha. The goal of this study was to investigate the potential role of IL-22 in liver regeneration after 70% hepatectomy. Following 70% hepatectomy, done under general anesthesia in mice, serum IL-22 and hepatic IL-22Ralpha mRNA were significantly increased. Although administration of exogenous IL-22 prior to hepatectomy did not increase hepatocyte proliferation, administration of anti-IL-22 antibody before hepatectomy did significantly decrease hepatocyte proliferation. Furthermore, IL-22 treatment prior to 70% hepatectomy induced stat-3 activation; no significant changes were seen in ERK1/2 activation, stat-1 activation, or stat-5 activation. IL-22 pretreatment also significantly increased hepatic and serum IL-6 levels. In addition, animals treated with anti-IL-22 antibody also expressed less TGF-alpha. In conclusion, these data suggest that IL-22 is involved in liver regeneration and this may be due to interaction with IL-6 and TGF-alpha cascades.
authors.affiliation: Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan, USA.
authors.forename: Xiaodan
authors.initials: X
authors.lastname: Ren
authors.forename: Bin
authors.initials: B
authors.lastname: Hu
authors.forename: Lisa M
authors.initials: LM
authors.lastname: Colletti
mesh_terms: D000818:Animals; D002455:Cell Division / Q000187:drug effects; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D005260:Female; D006498:Hepatectomy / Q000379:methods*; D017228:Hepatocyte Growth Factor / Q000378:metabolism; D022781:Hepatocytes / Q000166:cytology / Q000187:drug effects; D015850:Interleukin-6 / Q000378:metabolism; D007378:Interleukins / Q000235:genetics* / Q000378:metabolism* / Q000494:pharmacology; D008099:Liver / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D008115:Liver Regeneration / Q000187:drug effects / Q000502:physiology*; D020935:MAP Kinase Signaling System / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D010766:Phosphorylation / Q000502:physiology; D012333:RNA, Messenger / Q000378:metabolism; D018123:Receptors, Interleukin / Q000235:genetics / Q000378:metabolism; D011994:Recombinant Proteins / Q000378:metabolism / Q000494:pharmacology; D050794:STAT1 Transcription Factor / Q000378:metabolism; D050796:STAT3 Transcription Factor / Q000378:metabolism; D050799:STAT5 Transcription Factor / Q000378:metabolism; D016211:Transforming Growth Factor alpha / Q000378:metabolism; D015854:Up-Regulation / Q000502:physiology; D000097043:Interleukin-22
chemical_list: D048049:Extracellular Signal-Regulated MAP Kinases; D017228:Hepatocyte Growth Factor; D015850:Interleukin-6; D007378:Interleukins; D012333:RNA, Messenger; D018123:Receptors, Interleukin; D011994:Recombinant Proteins; D050794:STAT1 Transcription Factor; D050796:STAT3 Transcription Factor; D050799:STAT5 Transcription Factor; D016211:Transforming Growth Factor alpha; D000097043:Interleukin-22; C494080:Stat1 protein, mouse; C494087:Stat3 protein, mouse; C415369:interleukin-22 receptor