Cardioprotective Actions of the Annexin-A1 N-Terminal Peptide, Ac_2-26, Against Myocardial Infarction.

ABSTRACT: The anti-inflammatory, pro-resolving annexin-A1 protein acts as an endogenous brake against exaggerated cardiac necrosis, inflammation, and fibrosis following myocardial infarction (MI) in vivo. Little is known, however, regarding the cardioprotective actions of the N-terminal-derived peptide of annexin A1, Ac_2-26, particularly beyond its anti-necrotic actions in the first few hours after an ischemic insult. In this study, we tested the hypothesis that exogenous Ac_2-26 limits cardiac injury in vitro and in vivo. Firstly, we demonstrated that Ac_2-26 limits cardiomyocyte death both in vitro and in mice subjected to ischemia-reperfusion (I-R) injury in vivo (Ac_2-26, 1 mg/kg, i.v. just prior to post-ischemic reperfu

SUBMITTER: Qin CX 

PROVIDER: S-EPMC6457169 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature