Journal article

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

Cheng Xue Qin, Sarah Rosli, Minh Deo, Nga Cao, Jesse Walsh, Mitchel Tate, Amy E Alexander, Daniel Donner, Duncan Horlock, Renming Li, Helen Kiriazis, Man KS Lee, Jane E Bourke, Yuan Yang, Andrew J Murphy, Xiao-Jun Du, Xiao Ming Gao, Rebecca H Ritchie

Frontiers in Pharmacology | FRONTIERS MEDIA SA | Published : 2019


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, Ac2-26, particularly beyond its anti-necrotic actions in the first few hours after an ischemic insult. In this study, we tested the hypothesis that exogenous Ac2-26 limits cardiac injury in vitro and in vivo. Firstly, we demonstrated that Ac2-26 limits cardiomyocyte death both in vitro and in mice subjected to ischemia-reperfusion (I-R) injury in vivo (Ac2-26, 1 mg/kg, i.v. just prior to ..

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Awarded by National Health and Medical Research Council (NHMRC) of Australia

Awarded by NHMRC

Funding Acknowledgements

This work was supported in part by both the National Health and Medical Research Council (NHMRC) of Australia, including APP1045140 (to RR, XG, and YY), and the Victorian Government's Operational Infrastructure Support Program. RR and X-JD are NHMRC Senior Research Fellows (APP1059960 and APP1043026 respectively), CQ is a Baker Fellow. AM was supported Centenary Award from CSL. ML was supported by a post-doctoral fellowship from the National Heart Foundation.