Abstract
This study tested the hypothesis that extracorporeal shock wave- (ECSW-) assisted adipose-derived stromal vascular fraction (SVF) therapy could preserve left ventricular ejection fraction (LVEF) and inhibit LV remodeling in a rat after acute myocardial infarction (AMI). Adult male SD rats were categorized into group 1 (sham control), group 2 (AMI induced by left coronary artery ligation), group 3 [AMI + ECSW (280 impulses at 0.1 mJ/mm2, applied to the chest wall at 3 h, days 3 and 7 after AMI), group 4 [AMI + SVF (1.2 × 106) implanted into the infarct area at 3 h after AMI], and group 5 (AMI + ECSW-SVF). In vitro, SVF protected H9C2 cells against menadione-induced mitochondrial damage and increased fluorescent intensity of mitochondria in nuclei (p < 0.01). By day 42 after AMI, LVEF was highest in group 1, lowest in group 2, significantly higher in group 5 than in groups 3 and 4, and similar between the latter two groups (all p < 0.0001). LV remodeling and infarcted, fibrotic, and collagen deposition areas as well as apoptotic nuclei exhibited an opposite pattern to LVEF among the groups (all p < 0.0001). Protein expressions of CD31/vWF/eNOS/PGC-1α/α-MHC/mitochondrial cytochrome C exhibited an identical pattern, whilst protein expressions of MMP-9/TNF-α/IL-1β/NF-κB/caspase-3/PARP/Samd3/TGF-β/NOX-1/NOX-2/oxidized protein/β-MHC/BNP exhibited an opposite pattern to LVEF among five groups (all p < 0.0001). Cellular expressions of CXCR4/SDF-1α/Sca-1/c-Kit significantly and progressively increased from groups 1 to 5 (all p < 0.0001). Cellular expression of γ-H2AX/CD68 displayed an opposite pattern to LVEF among the five groups (all p < 0.0001). In conclusion, ECSW-SVF therapy effectively preserved LVEF and inhibited LV remodeling in rat AMI.
Highlights
Even undergoing rapid reperfusion therapy [1,2,3,4,5], acute myocardial infarction (AMI) causes muscle death pump failure
By day 14 after AMI, left ventricular enddiastolic diameter (LVEDd) was significantly higher in AMI than in other four groups, significantly higher in AMI-Extracorporeal shock wave (ECSW) and AMI-stromal vascular fraction (SVF) than in sham-operated control (SC) and AMI-ECSWSVF, but it showed no difference between the latter two groups or among AMI-ECSW, AMI-SVF, and AMI-ECSWSVF
left ventricular end-systolic diameter (LVESd) was highest in AMI and lowest in SC, significantly higher in AMI-ECSW and AMI-SVF than in AMI-ECSW-SVF, but similar between AMI-ECSW and AMI-SVF
Summary
Even undergoing rapid reperfusion therapy [1,2,3,4,5], acute myocardial infarction (AMI) causes muscle death pump failure. Abundant data supports that stem cell therapy can improve ischemia-related organ dysfunction, for cardiovascular diseases, including AMI [6,7,8,9,10]. Most experimental or clinical trials indicate that an adequate number of stem cells are essential for ischemia-related organ dysfunction to be treated successfully [6, 11,12,13]. Stem cell culture and expansion are necessary [14,15,16], but these take too long for AMI patients for whom rapid treatment is critical. An innovative method that could provide adequate stem cells quickly without cell culture and be effective as a treatment for AMI would be of great clinical importance
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