{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T23:10:54Z","timestamp":1777417854492,"version":"3.51.4"},"reference-count":50,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","license":[{"start":{"date-parts":[[2020,11,2]],"date-time":"2020-11-02T00:00:00Z","timestamp":1604275200000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Hepatology"],"published-print":{"date-parts":[[2021,2]]},"abstract":"<jats:sec>\n            <jats:title>Background and Aims<\/jats:title>\n            <jats:p>Growth hormone (GH) is important for liver regeneration after partial hepatectomy (PHx). We investigated this process in C57BL\/6 mice that express different forms of the GH receptor (GHR) with deletions in key signaling domains.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results<\/jats:title>\n            <jats:p>PHx was performed on C57BL\/6 mice lacking GHR (<jats:italic toggle=\"yes\">Ghr<\/jats:italic>\n                                 <jats:sup>\u2212\/\u2212<\/jats:sup>), disabled for all GH\u2010dependent Janus kinase 2 signaling (<jats:italic toggle=\"yes\">Box1<\/jats:italic>\n                                 <jats:sup>\u2212\/\u2212<\/jats:sup>), or lacking only GH\u2010dependent signal transducer and activator of transcription 5 (STAT5) signaling (<jats:italic toggle=\"yes\">Ghr391<\/jats:italic>\n                                 <jats:sup>\u2212\/\u2212<\/jats:sup>), and wild\u2010type littermates. C57BL\/6 <jats:italic toggle=\"yes\">Ghr<\/jats:italic>\n                                 <jats:sup>\u2212\/\u2212<\/jats:sup>mice showed striking mortality within 48\u00a0hours after PHx, whereas <jats:italic toggle=\"yes\">Box1<\/jats:italic>\n                                 <jats:sup>\u2212\/\u2212<\/jats:sup> or <jats:italic toggle=\"yes\">Ghr391<\/jats:italic>\n                                 <jats:sup>\u2212\/\u2212<\/jats:sup> mice survived with normal liver regeneration. <jats:italic toggle=\"yes\">Ghr<\/jats:italic>\n                                 <jats:sup>\u2212\/\u2212<\/jats:sup> mortality was associated with increased apoptosis and elevated natural killer\/natural killer T cell and macrophage cell markers. We identified H2\u2010Bl, a key immunotolerance protein, which is up\u2010regulated by PHx through a GH\u2010mediated, Janus kinase 2\u2013independent, SRC family kinase\u2013dependent pathway. GH treatment was confirmed to up\u2010regulate expression of the human homolog of <jats:italic toggle=\"yes\">H2\u2010Bl<\/jats:italic> (human leukocyte antigen G [<jats:italic toggle=\"yes\">HLA\u2010G<\/jats:italic>]) in primary human hepatocytes and in the serum of GH\u2010deficient patients. We find that injury\u2010associated innate immune attack by natural killer\/natural killer T cell and macrophage cells are instrumental in the failure of liver regeneration, and this can be overcome in <jats:italic toggle=\"yes\">Ghr<\/jats:italic>\n                                 <jats:sup>\u2212\/\u2212<\/jats:sup> mice by adenoviral delivery of H2\u2010Bl or by infusion of HLA\u2010G protein. Further, H2\u2010Bl knockdown in wild\u2010type C57BL\/6 mice showed elevated markers of inflammation after PHx, whereas <jats:italic toggle=\"yes\">Ghr<\/jats:italic>\n                                 <jats:sup>\u2212\/\u2212<\/jats:sup> backcrossed on a strain with high endogenous <jats:italic toggle=\"yes\">H2<\/jats:italic>\u2010<jats:italic toggle=\"yes\">Bl<\/jats:italic> expression showed a high rate of survival following PHx.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>GH induction of <jats:italic toggle=\"yes\">H2\u2010Bl<\/jats:italic> expression is crucial for reducing innate immune\u2010mediated apoptosis and promoting survival after PHx in C57BL\/6 mice. Treatment with HLA\u2010G may lead to improved clinical outcomes following liver surgery or transplantation.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.31297","type":"journal-article","created":{"date-parts":[[2020,4,28]],"date-time":"2020-04-28T02:13:04Z","timestamp":1588039984000},"page":"759-775","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":30,"title":["Growth Hormone Stops Excessive Inflammation After Partial Hepatectomy, Allowing Liver Regeneration and Survival Through Induction of H2\u2010Bl\/HLA\u2010G"],"prefix":"10.1097","volume":"73","author":[{"given":"Mayumi","family":"Ishikawa","sequence":"first","affiliation":[{"name":"Institute for Molecular Bioscience,The University of Queensland,St. Lucia,QLD,Australia"},{"name":"Center for Endocrinology, Diabetes and Arteriosclerosis,Nippon Medical School Musashikosugi 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