Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5888322 | Experimental and Molecular Pathology | 2014 | 8 Pages |
Abstract
Cell therapy has emerged as an attractive therapeutic modality to treat myocardial infarction (MI) via repairing damaged myocardium, and mesenchymal stem cells (MSCs) are an appealing therapeutic approach for cardiac regeneration. However, the clinical application of MSC-based therapy is restricted because of the poor survival of implanted cells, and this poor survival remains poorly understood. Using a tumor necrosis factor (TNF)-α-induced bone marrow (BM)-MSC injury model in vitro and a rat MI model in vivo, we showed in the current study that miR-23a was involved in TNF-α-induced BM-MSC apoptosis through regulating caspase-7 and that the injection of BM-MSCs overexpressing miR-23a could improve left ventricular (LV) function and reduce infarct size in the rat MI model. Our findings elucidate the etiology of MI and provide an alternative treatment strategy for patients with heart failure caused by MI who are not optimal candidates for surgical treatment.
Keywords
EDDIVSHSCsLV end-diastolic diameterESDTTCAARLV end-systolic diameterMSCsLVDsmiRNAsLVDdTNFNF-κBMyocardial infarctionEnd-diastolic dimensionLeft ventricularEnd-systolic dimensionTriphenyltetrazolium chlorideTUNELApoptosismicroRNAshematopoietic stem cellsMesenchymal stem cellstumor necrosis factornuclear factor κBLADSerum deprivationbone marrowarea at riskMicroRNAleft anterior descending arterycaspasefractional shortening
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Authors
Jianqiang Mao, Zhiqian Lv, Yu Zhuang,