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.
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.
Methods: 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 NPY-treated 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.