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Updated: Feb 23, 2026
In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge
Published on: June 15, 2018
Overexpressed microRNA-506 and microRNA-124 alleviate H2O2-induced human cardiomyocyte dysfunction by targeting
Xiuzhou Zhang1, Fuyan Liu2, Qingqing Wang3
1Department of Cardiology, Binzhou People's Hospital, Binzhou, Shandong 256610, P.R. China.
Abstract:
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 H2O2-induced human cardiomyocyte (HCM) injury. In H2O2‑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 H2O2 induced significant apoptosis and increased the concentration of reactive oxygen species (ROS) in HCMs. H2O2 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 H2O2‑induced upregulation of KLF4 and KLF5 in the HCMs. The overexpression of miR‑506 and miR‑214 reversed the H2O2‑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 H2O2‑induced HCM injury by suppressing the expression of KLF4 and KLF5.
Insights
MicroRNAs miR-506 and miR-214 protect human cardiomyocytes from injury by reducing oxidative stress and apoptosis. They achieve this by suppressing Krüppel-like factors KLF4 and KLF5 expression.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Cellular Pathology
Background:
- Krüppel-like factors (KLFs) are crucial regulators of cellular functions and disease processes.
- MicroRNAs (miRs) play significant roles in post-transcriptional gene regulation.
- Hydrogen peroxide (H2O2) is a known inducer of oxidative stress and apoptosis in human cardiomyocytes (HCMs).
Purpose of the Study:
- To investigate the role of microRNAs (miRs) in H2O2-induced human cardiomyocyte (HCM) injury.
- To elucidate the post-translational regulatory mechanisms involving miRs and KLFs in cardiac injury.
- To determine the protective effects of specific miRs against H2O2-induced oxidative stress and apoptosis in HCMs.
Main Methods:
- H2O2-induced HCM injury model.
- Flow cytometry for reactive oxygen species (ROS) and apoptosis assessment.
- Transfection with miR mimics and inhibitors.
- MTT assay for cell proliferation.
- Bioinformatics prediction and dual luciferase reporter assay for target gene validation.
- Reverse transcription-polymerase chain reaction and western blotting for gene and protein expression analysis.
Main Results:
- H2O2 exposure significantly increased apoptosis and ROS levels in HCMs.
- H2O2 upregulated KLF4 and KLF5 expression while downregulating miR-506 and miR-124.
- miR-506 and miR-124 directly target KLF4 and KLF5, respectively.
- Overexpression of miR-506 and miR-124 attenuated H2O2-induced KLF4/KLF5 upregulation.
- Overexpression of miR-506 and miR-214 reversed H2O2-induced apoptosis and ROS increase.
Conclusions:
- miR-506 and miR-214 demonstrate a protective effect against H2O2-induced HCM injury.
- This protection is mediated by the suppression of KLF4 and KLF5 expression.
- These findings highlight a novel therapeutic pathway for managing cardiac injury involving oxidative stress.
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