Conclusion
The miR-542-3p can negatively regulate PDE4D protein expression and attenuate cardiomyocyte injury through a mechanism related to the activation of the cAMP/PKA signaling pathway.
Methods
A cardiomyocyte hypoxia/reoxygenation model was established. The expression levels of miR-542-3p and PDE4D were detected using qRT-PCR; the luciferase reporter assay system was used to detect the targeting relationship between miR-542-3p and PDE4D; overexpressing miR-542-3p was transfected into cardiomyocytes, and ROS release was detected by immunofluorescence while cellular apoptosis was detected by TUNEL; and the western blot assay was applied to detect the expression of PDE4D, phosphorylated protein kinase A (p-PKA), and phosphorylated cyclic adenosine monophosphate (cAMP) response element-binding protein (p-CREB).
Objective
To investigate the protective effect of miR-542-3p on cardiomyocyte injury and related mechanisms.
Results
Compared with the control group, the miR-542-3p expression level was decreased and the PDE4D expression level was increased in the cardiomyocyte hypoxia/reoxygenation model group. The dual-luciferase reporter assay system confirmed that miR-542-3p could target and regulate PDE4D; the transfection with cardiomyocytes using the overexpressing miR-542-3p could downregulate PDE4D expression, attenuate ROS release during cardiomyocyte injury, and reduce cellular apoptosis rate, while upregulating the expression of p-PKA and p-CREB.