Neuropeptide Y Induces Cardiomyocyte Hypertrophy via Attenuating miR-29a-3p in Neonatal Rat Cardiomyocytes

Abstract

Background: Neuropeptide Y (NPY) has been well known to induce cardiomyocyte hypertrophy (CH), which is possibly caused by disruption of cardiac cell energy balance. As mitochondria is losely related to energy metabolism, in this study, we investigated the changes in mitochondrial dynamics-related protein (Drp1) expression under the action of NPY. miRNA-29a, a endogenous noncoding small molecule RNA which is involved in many cardiac diseases, by using a bioinformatics tool, we found a potential binding site of miRNA-29a on the Drp1 mRNA, and suggesting that miRNA-29a might play a regulatory role. Methods: Objective: To investigate the role of miR-29a-3p in the process of NPY-induced CH, and further explore it’s predicted relationship with Drp1. The expression levels of miR-29a-3p and atrial natriuretic peptide (ANP) were performed by the method of fluorescence quantitative PCR, in addition, expression of Drp1 in treated and control groups were performed by western blot analysis. Results: We found NPY leads to the CH and up-regulation of ANP expression levels. We also found significant up-regulation of Drp1 expression and down-regulation of miR-29a-3p expression in NPYtreated cells. The decrease in miR-29a-3p expression may lead the increase expression level of Drp1. We found that the expression of ANP increased after NPY treatment. When Drp1 protein was silenced, the high expression of ANP was inhibited. Conclusion: In this study, we found up-regulation of Drp1 in cells treated with NPY. Drp1 mRNA is a predicted target for miR-29a-3p, and the expression of Drp1 was attenuated by miR-29a-3p. Therefore, NPY leads to down-regulation of miR-29a-3p expression, up-regulation of Drp1 expression, and NPY leads to CH. Correspondingly, miR-29a-3p can counteract the effects of NPY. This may be a new way, which could be used in diagnosis and treatment plan for CH.