Abstract
BackgroundRemote ischemic preconditioning (RIPC) has emerged as an attractive strategy in clinical settings. Despite convincing evidence of the critical role played by circulating humoral mediators, their actual identities remain unknown. In this study, we aimed to identify RIPC-induced humoral mediators using a proteomic approach.Methodsand Results Rats were exposed to 10-min limb ischemia followed by 5- (RIPC 5′) or 10-min (RIPC 10′) reperfusion prior to blood sampling. The control group only underwent blood sampling. Plasma samples were analyzed using surface-enhanced laser desorption and ionization - time of flight - mass spectrometry (SELDI-TOF-MS). Three protein peaks were selected for their significant increase in RIPC 10′. They were identified and confirmed as apolipoprotein A-I (ApoA-I). Additional rats were exposed to myocardial ischemia-reperfusion (I/R) and assigned to one of the following groups RIPC+myocardial infarction (MI) (10-min limb ischemia followed by 10-min reperfusion initiated 20 minutes prior to myocardial I/R), ApoA-I+MI (10 mg/kg ApoA-I injection 10 minutes before myocardial I/R), and MI (no further intervention). In comparison with untreated MI rats, RIPC reduced infarct size (52.2±3.7% in RIPC+MI vs. 64.9±2.6% in MI; p<0.05). Similarly, ApoA-I injection decreased infarct size (50.9±3.8%; p<0.05 vs. MI).ConclusionsRIPC was associated with a plasmatic increase in ApoA-I. Furthermore, ApoA-I injection before myocardial I/R recapitulated the cardioprotection offered by RIPC in rats. This data suggests that ApoA-I may be a protective blood-borne factor involved in the RIPC mechanism.
Highlights
Local ischemic preconditioning, which consists of transient nonlethal episodes of myocardial ischemia before a prolonged ischemia-reperfusion (I/R) cardiac injury, is well recognized as one of the most potent innate cardioprotective mechanisms
With no need for invasive procedures, Remote ischemic preconditioning (RIPC) using transient limb ischemia as a stimulus has emerged as an attractive strategy in clinical settings [2,7]
From a total of 207 peaks detected for lowmass proteins (89 for CM10, 118 for H50) and 164 peaks for highmass proteins (74 for CM10, 90 for H50), 30 SELDI peaks displayed significant modulation relative to their RIPC groups, with 15 being increased and 15 decreased
Summary
Local ischemic preconditioning, which consists of transient nonlethal episodes of myocardial ischemia before a prolonged ischemia-reperfusion (I/R) cardiac injury, is well recognized as one of the most potent innate cardioprotective mechanisms It necessitates direct application of invasive procedures to the myocardium in order to attain cardioprotection, which could be harmful in clinical settings. With no need for invasive procedures, RIPC using transient limb ischemia as a stimulus has emerged as an attractive strategy in clinical settings [2,7] This strategy was shown to attenuate myocardial injury in patients undergoing corrective cardiac surgery for congenital heart disease [8], coronary bypass surgery [9], elective surgery for abdominal aortic aneurysm [10], and elective percutaneous coronary interventions (PCI) [11]. We aimed to identify RIPC-induced humoral mediators using a proteomic approach
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