Hepatic Deletion of Janus Kinase 2 Counteracts Inflammation, Oxidative Stress and Liver Cancer Formation in Growth Hormone Transgenic Mice

ABSTRACT: Impairment of hepatic growth hormone (GH)- janus kinase (JAK) 2- signal transducer and activator of transcription (STAT) 5 signaling is associated with non-alcoholic fatty liver disease, while persistently high levels of GH can result in hepatic inflammation and liver cancer. Despite its anti-steatotic functions, STAT5 in hepatocytes has been implicated to be a tumor suppressor, whose loss strongly accelerates tumor formation in the presence of high GH levels. Yet, it remains unclear whether the upstream kinase JAK2 exerts similar tumor-suppressive functions. To address this question, we crossed a mouse model of inflammatory liver cancer (GHtg) to mice harboring the hepatocyte-specific deletion of JAK2 (JAK2Δhep) and compared them to GHtgSTAT5Δhep mice. We show that JAK2 deficiency in th

ORGANISM(S): Mus musculus

SUBMITTER: Madeleine Themanns 

PROVIDER: E-MTAB-3774 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress