FoxO4 promotes early inflammatory response upon myocardial infarction via endothelial Arg1.

ABSTRACT:

Rationale

Inflammation in post-myocardial infarction (MI) is necessary for myocyte repair and wound healing. Unfortunately, it is also a key component of subsequent heart failure pathology. Transcription factor forkhead box O4 (FoxO4) regulates a variety of biological processes, including inflammation. However, its role in MI remains unknown.

Objective

To test the hypothesis that FoxO4 promotes early post-MI inflammation via endothelial arginase 1 (Arg1).

Methods and results

We induced MI in wild-type and FoxO4(-/-) mice. FoxO4(-/-) mice had a significantly higher post-MI survival, better cardiac function, and reduced infarct size. FoxO4(-/-) hearts had significantly fewer neutrophils, reduced expression of cytokines, and competitive nitric oxide synthase inhibitor Ar

SUBMITTER: Zhu M 

PROVIDER: S-EPMC4710860 | biostudies-literature | 2015 Nov

REPOSITORIES: biostudies-literature