Therapeutic Efficacy Of MiR-133 Overexpressed BMSCs In Rats With Myocardial Infarction

Objective:Our study was toevaluate the therapeutic efficacy and mechanismsof miR-133-overexpressed BMSCs(Bone marrow mesenchymal stem cells) on myocardial infarction in ratsMethods :Rat BMSCs were isolated, purified by whole bone marrow adherent culturing, and their morphological characteristics were observed under the phase-contrast microscope.miR- 133- agomir(overexpression) and miR- 133 antagomir(suppress) was transfected by liposome 2000 transfectto regulate the expression of miR-133 inBMSCs. After transfection, BMSCs were collectedfor the assay ofcell apoptosis and proliferation. miR-133-overexpressed BMSCs were achievedby lenfiviral infection of miR-133. Rat myocardial infarction model was created by ligating the left anterior descending coronary artery. Then PBS or different BMSCs(PBS,normalBMSCs,BMSCs-pCDHvector,BMSCs-pCDH-miR-133) were injectedinto the zone around mycardial infarction. Myocardial function was evaluatedon days 7 and 28 post infarction. The infarcted hearts were collectedon day 28 to measure myocardial infarction area.Results: BMSCs apoptosis obviously reduced after miR- 133- agomir transfection.And snail1 expression in CMs also obviously decreased in co-cultive experiment with miR-133-overexpressed BMSCs.We successfully established the miR-133 lenfiviral vector and efficiently transfected BMSCs.Then we found that BMSCs-miR133 group can decrease the inflammation invasion level in the heart after acute myocardial infarction and obviously reduce the infarction area.Our study also found that group(BMSCs-pCDH-mi R-133) plays a significant role of relieving myocardial infarction, and promoted the improvement of the cardiac function.Conclusion:mi R- 133 overexpression was able to inhibit cell apoptosis in BMSCs. Our study successfully established the mi R-133-overexpressed BMSCs.We found BMSCs-miR-133 can obviously reduce mycardial infarction area and improve cardiac function after myocardial infarction.This phenomoenon may be caused by the decrese of BMSCs’ apotosis and inhibition of snail1 expression in cardiac myocyte. Thus,our study provided a theoretical basis for the further applyment of gene-modified BMSCs for the treatment of relevant diseases.