Hepatic Deletion of Janus Kinase 2 Counteracts Oxidative Stress in Mice.

ABSTRACT: Genetic deletion of the tyrosine kinase JAK2 or the downstream transcription factor STAT5 in liver impairs growth hormone (GH) signalling and thereby promotes fatty liver disease. Hepatic STAT5 deficiency accelerates liver tumourigenesis in presence of high GH levels. To determine whether the upstream kinase JAK2 exerts similar functions, we crossed mice harbouring a hepatocyte-specific deletion of JAK2 (JAK2^Δhep) to GH transgenic mice (GH^tg) and compared them to GH^tgSTAT5^Δhep mice. Similar to GH^tgSTAT5^Δhep mice, JAK2 deficiency resulted in severe steatosis in the GH^tg background. However, in contrast to STAT5 deficiency, loss of JAK2 significantly delayed liver tumourigenesis. This was attributed to: (i) activati

SUBMITTER: Themanns M 

PROVIDER: S-EPMC5054456 | biostudies-literature | 2016 Oct

REPOSITORIES: biostudies-literature