Ischemic postconditioning (PoCo) reduces
infarct size following
myocardial ischemia/reperfusion. To protect, PoCo must be performed early during reperfusion, and causal cardioprotective signaling must occur then. The role of
microRNA (
miRNA) in PoCo is unclear. Anesthetized pigs were subjected to 60 min left anterior descending coronary artery (LAD) occlusion and 180 min reperfusion. Immediate full reperfusion (IFR, n = 5) was compared to PoCo (four cycles of 60 s/60 s reperfusion/reocclusion, n = 5). Transmural myocardial biopsies from the LAD territory were sampled at baseline, 60 min
ischemia, 10 and 180 min reperfusion.
RNA was isolated. The expression of 11
miRNAs, including muscle-specific (miRNA-1, -133a, -206, -208b, -214, and -499),
fibrosis- (miRNA-21, -24, and -29b), neovascularization- (miRNA-92a), and
inflammation-associated (miRNA-146b) candidates, was quantified using real-time PCR (RT-PCR).
mRNA expression at baseline and 180 min reperfusion was quantified and validated (microarray and RT-PCR). PoCo reduced
infarct size from 44.9 ± 7.7 to 34.8 ± 5.3% of the area at risk. The expression of miRNA-1, -24, -29b, -133a, -146b, -208b, and -499 was increased
at 10 min reperfusion with PoCo vs. IFR; however, that of miRNA-1, -24, -208b, and -499 was already increased at 60 min
ischemia and probably reflects falsely positive results. Five mRNAs were different with PoCo vs. IFR. In silico analysis identified a tentative connection between three
miRNAs and five mRNAs with the
biological functions "cell death", "inflammatory response" and/or "
glucose metabolism". If at all, only miRNA-29b, -133a, and -146b fulfill the minimal temporal requirements for a potential causal involvement in cardioprotection by PoCo.