miR-19a mitigates hypoxia/reoxygenation-induced injury by depressing CCL20 and inactivating MAPK pathway in human embryonic cardiomyocytes.

Myocardial infarction (MI) is a prevalent cardiovascular puzzle and a mainspring of disease-induced mortality. We performed this investigation to detect the role of putative important miRNAs or genes in MI. CCL20 may be a potential therapeutic target, which was directly targeted and negatively regulated by miR-19a. CCL20 expression was significantly increased in MI tissue samples, but miR-19a was expressed at lower levels in MI. H/R treatment inhibited cell viability and induced an increase of apoptotic rate compared with Sham group. However, miR-19a mimic relieved the H/R-stimulated injury to cardiomyocytes. Protective effect of miR-19a against H/R in cardiomyocytes was reversed by CCL20 enhancement, and MAPK pathway was inactivated during this progression. miR-19a eliminates the H/R-induced injury in cardiomyocytes through directly targeting CCL20 and attenuating the activity of MAPK signaling pathway. These observations highlighted the therapeutic roles of miR-19a and CCL20 for MI treatment.