Helium Postconditioning Regulates Caveolin‐1/‐3 Translocation and Gene Expression

Abstract

Caveolae, lipid enriched invaginations of the plasma membrane, are epicentres of cellular signal transduction. Caveolins, structural proteins localized to caveolae, have been shown to play an important role in anesthetic‐induced cardioprotection. Helium (He) postconditioning is known to reduce infarct size and induces cardioprotection. We here hypothesize that He postconditioning regulates caveolin‐1 and ‐3 (Cav‐1 and Cav‐3) in the heart. Employing coronary artery occlusion, male Wistar rats (n=8 each group) were subjected to 25 min of cardiac ischemia and reperfusion (I/R) for 5, 15 or 30 min (I/R 5/15/30), respectively. The He postconditioning groups underwent I/R plus 70% He during reperfusion (He 5/15/30 minutes, respectively). The sham group received surgical treatment without I/R (Sham). After each protocol blood and hearts were retrieved. The tissue was obtained from the area at risk (AAR) and the non‐area at risk (NAAR) and processed for Western blot analyses and qRT‐PCR. The membrane fraction (AAR) of He 15 showed increased levels of Cav‐1 (p<0.05 vs. I/R 15) and Cav‐3 (p<0.05 vs. I/R 15). Elevated levels of Cav‐3 were also found in the He 15 serum (p<0.05 vs. I/R 15). Gene expression analyses revealed decreased expression of Cav‐3 in He 15 compared to Sham in AAR (p<0.05) and NAAR (p<0.05) tissue. These data suggest that 15 min He postconditioning might induce survival pathways by regulating caveolin‐1/‐3 translocation and gene expression.This study was funded by the SCA.