Transgenic overexpression of GTP cyclohydrolase 1 in cardiomyocytes ameliorates post-infarction cardiac remodeling.

ABSTRACT: GTP cyclohydrolase 1 (GCH1) and its product tetrahydrobiopterin play crucial roles in cardiovascular health and disease, yet the exact regulation and role of GCH1 in adverse cardiac remodeling after myocardial infarction are still enigmatic. Here we report that cardiac GCH1 is degraded in remodeled hearts after myocardial infarction, concomitant with increases in the thickness of interventricular septum, interstitial fibrosis, and phosphorylated p38 mitogen-activated protein kinase and decreases in left ventricular anterior wall thickness, cardiac contractility, tetrahydrobiopterin, the dimers of nitric oxide synthase, sarcoplasmic reticulum Ca²⁺ release, and the expression of sarcoplasmic reticulum Ca²⁺ handling proteins. Intriguingly, transgenic overexpression of GC

SUBMITTER: Liu Y 

PROVIDER: S-EPMC5465102 | biostudies-literature | 2017 Jun

REPOSITORIES: biostudies-literature