miR-208a Promotes Apoptosis in H9c2 Cardiomyocytes by Targeting GATA4

Background: microRNAs are crucial for cardiovascular development and associated with congenital heart disease (CHD). Recent studies have shown that play a role in is closely related to CHD. The present study investigated the underlying mechanism of microRNA-208a (miR-208a) “simple” Material Methods: Reverse transcription-quantitative PCR (RT-qPCR) demonstrated miR-208a expression levels children CHD (n = 27) compared normal controls 29), cardiomyocytes from embryo 10 (E10) post-birth (P7) organs adult rats healthy rats. Apoptosis H9c2 cells after transfection detected by TUNEL assay. B-cell lymphoma (Bcl)-2, an anti-apoptotic gene, was RT-qPCR, as well Gata4. After 48h overexpression miR-208a, GATA4 via western blotting. Dual luciferase reporting system used identify binding sites Results: Expression upregulated group control (p < 0.01). At P7, had highest 0.01), which myocardiocytes other or tissues 0.01) number apoptotic increased significantly post-transfection while decreased inhibitor Compared group, there no significant difference level Bcl-2 > 0.05). proved binds directly 3´-UTR Gata4 at site 1,363-1,369 bp. but following Conclusions: Our downregulates targeting GATA4, may cause become new biomarker therapeutic target future.