Stat3β mitigates development of atherosclerosis in apolipoprotein E-deficient mice.

ABSTRACT: The transcription factor Stat3 is an activator of systemic inflammatory genes. Two isoforms of Stat3 are generated by alternative splicing, Stat3α and Stat3β. The β isoform lacks the transactivation domain but retains other functions, including dimerization and DNA binding. Stat3β-deficient mice exhibit elevated expression of systemic inflammatory genes and are hyperresponsive to lipopolysaccharide, suggesting that Stat3β functions predominantly as a suppressor of systemic inflammation. To test whether Stat3β deficiency would provoke pathologic effects associated with chronic inflammation, we asked whether selective removal of Stat3β would exacerbate the development of atherosclerosis in apolipoprotein E-deficient mice. In apoE(-/-)Stat3β(-/-) mice atherosclerotic plaque formation was sign

SUBMITTER: Lee J 

PROVIDER: S-EPMC3739303 | biostudies-literature | 2013 Aug

REPOSITORIES: biostudies-literature