miR-200a-3p regulates gene expression of diabetic cardiomyopathy in murine cardiomyocytes

Hsa-miR200a-3p play a crucial role in regulating glycometabolism and diabetic progression. But how hsa-miR200a-3p impact diabetic cardiomyopathy development is sitill ill-defined. Here,we found that the expression of hsa-miR200a-3p was significantly reduced in mouse cardiomyocytes HL-1 cells after high glucose stimulation. And we systemically investigated the overall mRNA expression level under hsa-miR200a-3p mimics, or inhibitors treatment in HL-1 at high glucose conditions. High-throughput sequencing results showed that 744 genes were significantly differentially expressed by high glucose stimulation in mouse cardiomyocytes. And when compared with the control group, 414 genes were differentially expressed after hsa-miR200a-3p overexpression; 33 genes were differentially expressed after added hsa-miR200a-3p inhibitor. WGCNA analysis found that all DEGs could be divided into five modules, and the gene expression pattern in the yellow module was positively correlated with hsa-miR200a-3p overexpression group and negatively correlated with hsa-miR200a-3p inhibitor group.We observed that these DEGs were mostly enriched in RrRNA processing, translation, and RNA transport. Then, we further identified three DEGs (Gm13205, Flnc, and Ntmt1) were found to be commonly expressed in down-regulated DEGs of the hsa-miR200a-3p mimics group and up-regulated DEGs of the hsa-miR200a-3p inhibitor/ high glucose groups. In addition, we predicted that Srm andTspan4 were two main targets for hsa-miR200a-3p in HL-1 cells. These findings demonstrate that high glucose suppressed hsa-miR200a-3p in vitro, and hsa-miR200a-3p may involve in diabetic cardiomyopathy development.