This study explores the mechanism of miR-36a in the hypoxia-reoxygenation process and its engagement in the repair of cardiomyocytes via modulating bone marrow mesenchymal stem cells (BMSCs). Thirty-two patients with myocardial injury were enrolled after hospitalization. Meanwhile,
32 normal patients were recruited as controls. The miR-36a levels were quantified via ELISA. BMSCs were isolated and cultured. The qRT-PCR was employed to determine the expression of genes involved in myocardial injury and hypoxia-reoxygenation, including KGF, SpB, SpA, CK18, SpC and Occludin.
Specific mRNAs related to myocardial damage repair were also measured after miR-36a was knockdown and overexpressed during the process of repair induction. The expression of miR-36a in 32 patients with myocardial injury was elevated compared to that in controls. BMSCs can quantitatively retard
the expression of hypoxia-reoxygenation-related genes. The knockdown of miR-36a can significantly enhance the expression of hypoxia-reoxygenation-related genes which were engaged in myocardial injury. miR-36a overexpression can significantly impede the expression of the hypoxia-reoxygenation-related
genes which were involved in myocardial injury. miR-36a contributes to the repair of myocardial injury via functionally enhancing BMSCs’ function and interfering with the hypoxia-reoxygenation process.
Bone marrow mesenchymal stem cells alleviate the daunorubicin-induced subacute myocardial injury in rats through inhibiting infiltration of T lymphocytes and antigen-presenting cells
