Overexpressed microRNA-506 and microRNA-124 alleviate H(2)O(2)-induced human cardiomyocyte dysfunction by targeting krüppel-like factor 4/5

Krüppel-like factors (KLFs) regulate a wide variety of cellular functions and modulate pathological processes. In the present study, a post-translational mechanism of microRNAs (miRs) was investigated in H(2)O(2)-induced human cardiomyocyte (HCM) injury. In H(2)O(2)-cultured HCM cells, reactive oxygen species and apoptotic cells were measured via flow cytometry. miR-506/-124 mimics and inhibitors were transfected to induce gain or loss of miR-506/-124 function. Cell proliferation was analyzed by an MTT assay. The targeted genes were predicted by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay. The mRNA and protein expression levels were measured by reverse transcription-polymerse chain reaction analysis and western blotting, respectively. The results indicated that H(2)O(2) induced significant apoptosis and increased the concentration of reactive oxygen species (ROS) in HCMs. H(2)O(2) markedly upregulated the expression levels of KLF4 and KLF5, and downregulated the expression levels of miR-506 and miR-124 in the HCMs. In addition, bioinformatics analysis showed the potential miR-506 and miR-124 binding sites within the 3′-untranslated region of KLF4 and KLF5 in the HCMs. The overexpression of miR-506 and miR-124 inhibited the H(2)O(2)-induced upregulation of KLF4 and KLF5 in the HCMs. The overexpression of miR-506 and miR-214 reversed the H(2)O(2)-induced apoptosis and increase of ROS in the HCMs. In conclusion, the overexpression of miR-506 and miR-214 were confirmed to have a protective effect against H(2)O(2)-induced HCM injury by suppressing the expression of KLF4 and KLF5.