Knockdown of Mir-1275 Protects Against Cardiomyocytes Injury Through Promoting Neuromedin U Type 1 Receptor

The present study aimed to assess the role of miR-1275 in cardiac ischemia reperfusion injury. H9 human embryonic stem cell (hESC)-derived cardiomyocytes stimulated by oxygen-glucose deprivation/reoxygenation (OGD/R) were used to simulate myocardial injury in vitro. miR-1275 expression levels in cells were measured by RT-qPCR. The release of lactate dehydrogenase (LDH) and creatine kinase (CK) was examined through LDH and CK ELISA kits. Cell apoptosis was detected through flow cytometry. A Fura-2 Calcium Flux Assay Kit and a Fluo-4 assay kit were used to determine the Ca2+ concentration. Expression levels of proteins were tested by Western blotting. The binding effect of miR-1275 and neuromedin U type 1 receptor (NMUR1) was detected by dual-luciferase activity assay. The results showed that miR-1275 was upregulated in OGD/R-stimulated cardiomyocytes. Inhibition of miR-1275 suppressed the increased activity of LDH and CK, cell apoptosis, reactive oxygen species (ROS) production, intracellular Ca2+ concentration and sarcoplasmic reticulum (SR) Ca2+ leak induced by OGD/R treatment in cardiomyocytes. miR-1275 directly targets 3'UTR of NMUR1 and negatively regulates NMUR1 expression. Silence of NMUR1 abolished the protecting effect of the miR-1275 antagomir on myocardial OGD/R injury. Our study indicated that the miR-1275 antagomir protects cardiomyocytes from OGD/R injury through the promotion of NMUR1.