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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 reperfusion). Further, Ac 2-26  (1 mg/kg i.v.) reduced cardiac inflammation (after 48 h reperfusion), as well as both cardiac fibrosis and apoptosis (after 7-days reperfusion). Lastly, we investigated whether Ac 2-26  preserved cardiac function after MI. Ac 2-26  (1 mg/kg/day s.c., osmotic pump) delayed early cardiac dysfunction 1 week post MI, but elicited no further improvement 4 weeks after MI. Taken together, our data demonstrate the first evidence that Ac 2-26  not only preserves cardiomyocyte survival  in vitro , but also offers cardioprotection beyond the first few hours after an ischemic insult  in vivo . Annexin-A1 mimetics thus represent a potential new therapy to improve cardiac outcomes after MI.

Cardioprotective Actions of the Annexin-A1 N-Terminal Peptide, Ac2-26, Against Myocardial Infarction