Journal article
Reperfusion-induced myocardial dysfunction is prevented by endogenous annexin-A1 and its N-terminal-derived peptide Ac-ANX-A12-26
C Qin, KD Buxton, S Pepe, AH Cao, K Venardos, JE Love, DM Kaye, YH Yang, EF Morand, RH Ritchie
British Journal of Pharmacology | Published : 2013
Abstract
Background and Purpose: Annexin-A1 (ANX-A1) is an endogenous, glucocorticoid-regulated anti-inflammatory protein. The N-terminal-derived peptide Ac-ANX-A12-26 preserves cardiomyocyte viability, but the impact of ANX-A1-peptides on cardiac contractility is unknown. We now test the hypothesis that ANX-A1 preserves post-ischaemic recovery of left ventricular (LV) function. Experimental Approach: Ac-ANX-A12-26 was administered on reperfusion, to adult rat cardiomyocytes as well as hearts isolated from rats, wild-type mice and mice deficient in endogenous ANX-A1 (ANX-A1 -/-). Myocardial viability and recovery of LV function were determined. Key Results: Ischaemia-reperfusion markedly impaired bot..
View full abstractGrants
Awarded by National Heart Foundation of Australia
Awarded by National Health and Medical Research Council of Australia
Funding Acknowledgements
This study was supported by the National Heart Foundation of Australia (grant-in-aid G 04 M 1529), the National Health and Medical Research Council of Australia (Senior Research Fellowship to RHR, ID472673) and supported in part by the Victorian Government's Operational Infrastructure Support Program.