MicroRNA-23a is involved in tumor necrosis factor-α induced apoptosis in mesenchymal stem cells and myocardial infarction

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. •TNF-α induces the apoptosis of BM-MSCs.•miR-23a protects against TNF-α-induced apoptosis in BM-MSCs.•Caspase-7 is the target gene of miR-23a in TNF-α-stimulated BM-MSCs.•miR-23a expression reduced cardiac damage after MI.