ArticleMedical science monitor : international medical journal of experimental and clinical research2020
MicroRNA-668-3p Protects Against Oxygen-Glucose Deprivation in a Rat H9c2 Cardiomyocyte Model of Ischemia-Reperfusion Injury by Targeting the Stromal Cell-Derived Factor-1 (SDF-1)/CXCR4 Signaling Pathway.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- MiR-668-5p targets ZNRF3, an E3 ubiquitin ligase to enhance osteoblast function and alleviate senescence in doxorubicin-induced age-related bone loss.Frontiers in endocrinology · 2025Article
- Targeting ferroptosis and ferritinophagy: new targets for cardiovascular diseases.Journal of Zhejiang University. Science. B · 2024Review
- MicroRNA-668-3p inhibits myoblast proliferation and differentiation by targeting Appl1.BMC genomics · 2023Article
- Exosomal miR-320e as a Novel Potential Biomarker for Cerebral Small Vessel Disease.International journal of general medicine · 2023Article
- The miR-668 binding site variant rs1046322 onFrontiers in endocrinology · 2023Article
- The Role of Hypoxia-Inducible Factor-1 Alpha in Renal Disease.Molecules (Basel, Switzerland) · 2022Review
- MicroRNA-668-3p regulates oxidative stress and cell damage induced by Aβ1-42 by targeting theAnnals of translational medicine · 2022Article
- Cardiac protection induced by urocortin-2 enables the regulation of apoptosis and fibrosis after ischemia and reperfusion involving miR-29a modulation.Molecular therapy. Nucleic acids · 2022Article
- Hypoxic/Ischemic Inflammation, MicroRNAs and δ-Opioid Receptors: Hypoxia/Ischemia-Sensitive Versus-Insensitive Organs.Frontiers in aging neuroscience · 2022Review
- microRNA-9-5p protects liver sinusoidal endothelial cell against oxygen glucose deprivation/reperfusion injury.Open life sciences · 2021Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Ischemia-reperfusion injury (IRI) results from the restoration of blood supply to ischemic organs, including the heart. Expression of microRNA-668-3p (miR-668-3p) is known to protect the kidney from IRI. This study aimed to investigate the role of miR-668-3p in oxygen-glucose deprivation (OGD) in a rat H9c2 cardiomyocyte model of IRI. MATERIAL AND METHODS Rat H9c2 cardiomyocytes were cultured in glucose-free Dulbecco's modified Eagle's medium (DMEM) under anaerobic conditions, followed by oxygenation, to create the OGD model of IRI. The luciferase reporter assay evaluated the interaction between stromal cell-derived factor-1 (SDF-1), or CXC motif chemokine 12 (CXCL12), and miR-668-3p. Protein and mRNA levels of SDF-1, CXCR4, Bcl2, Bax, cleaved caspase-3, endothelial nitric oxide synthase (eNOS), and phosphorylated endothelial nitric oxide synthase (p-eNOS) were analyzed by Western blot and quantitative reverse transcription-polymerase chain reaction (RT-qPCR), and apoptosis were assessed by flow cytometry. Enzyme-linked immunosorbent assay (ELISA) measured reactive oxygen species (ROS), including malondialdehyde (MDA), nitric oxide (NO), p-eNOS, and the inflammatory cytokines, tumor necrosis factor-alpha (TNF-alpha), interleukin-1ß (IL-1ß), IL-6, and monocyte chemoattractant protein-1 (MCP-1) in H9c2 cell supernatants. RESULTS In the OGD rat H9c2 cardiomyocyte model of IRI, miR-668-3p levels were reduced. Overexpression of miR-668-3p inhibited SDF-1, CXCR4, the expression of inflammatory cytokines, markers of oxidative stress, and p-eNOS. The overexpression of SDF-1 reversed these findings. Overexpression of SDF-1 promoted cell apoptosis, which was reduced by miR-668-3p. CONCLUSIONS In the OGD rat H9c2 cardiomyocyte model of IRI, miR-668-3p suppressed mediators of inflammation and oxidative stress and enhanced cell viability through the SDF-1/CXCR4 signaling pathway.
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