ArticleMolecular and cellular biochemistry2017
Extracellular vesicles-mediated transfer of miR-208a/b exaggerate hypoxia/reoxygenation injury in cardiomyocytes by reducing QKI expression.
Article in Molecular and cellular biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- The multifaceted roles of non-coding RNAs in cell-cell communication in cardiovascular health and disease.Cell & bioscience · 2025Review
- Identification of Connexin 26 on Extracellular Vesicles from Human Cardiomyocytes and Plasma: Novel Insights into miRNA Loading and Oxidative Injury.International journal of molecular sciences · 2025Article
- Exosome miRNA sorting controlled by RNA-binding protein-motif interactions.Extracellular vesicles and circulating nucleic acids · 2025Review
- Convergent accelerated evolution of mammal-specific conserved non-coding elements in hibernators.Scientific reports · 2024Article
- Cardiomyocyte intercellular signalling increases oxidative stress and reprograms the global- and phospho-proteome of cardiac fibroblasts.Journal of extracellular biology · 2023Article
- The RNA-binding protein QKI governs a muscle-specific alternative splicing program that shapes the contractile function of cardiomyocytes.Cardiovascular research · 2023Article
- Review
- SOCS6 Promotes Mitochondrial Fission and Cardiomyocyte Apoptosis and Is Negatively Regulated by Quaking-Mediated miR-19b.Oxidative medicine and cellular longevity · 2022Article
- QKI is a critical pre-mRNA alternative splicing regulator of cardiac myofibrillogenesis and contractile function.Nature communications · 2021Article
- The Emerging Roles of the RNA Binding Protein QKI in Cardiovascular Development and Function.Frontiers in cell and developmental biology · 2021Review
- RNA packaging into extracellular vesicles: An orchestra of RNA-binding proteins?Journal of extracellular vesicles · 2020Review
- Advances in Cardiovascular Biomarker Discovery.Biomedicines · 2020Review
- Hypoxia and extracellular vesicles: A review on methods, vesicular cargo and functions.Journal of extracellular vesicles · 2020Review
- A Roadmap for Fixing the Heart: RNA Regulatory Networks in Cardiac Disease.Molecular therapy. Nucleic acids · 2020Review
- Silencing of circHIPK3 Inhibits Pressure Overload-Induced Cardiac Hypertrophy and Dysfunction by Sponging miR-185-3p.Drug design, development and therapy · 2020Article
- miRNA-Coordinated Schizophrenia Risk Network Cross-Talk With Cardiovascular Repair and Opposed Gliomagenesis.Frontiers in genetics · 2020Article
- MiR-149 Aggravates Pyroptosis in Myocardial Ischemia-Reperfusion Damage via Silencing FoxO3.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- ACancer cell international · 2019Article
- Molecular functions and specific roles of circRNAs in the cardiovascular system.Non-coding RNA research · 2018Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we tested the hypothesis that extracellular vesicles (EVs)-mediated transfer of miR-208a/b can exacerbate apoptosis of cardiomyocytes (CMs) induced by hypoxia/reoxygenation (H/R) injury by reducing the expression of the RNA-binding protein Quaking (QKI). EVs were isolated from culture medium of hypoxic H9c2 cells (EVs-H). In in vitro H9c2 cell model, the EVs-H could be taken up by normoxic CMs and exacerbated cell apoptosis induced by H/R injury. In addition, miR-208a and miR-208b were enriched in EVs-H. Suppression of miR-208a and miR-208b loading significantly suppressed the detrimental effect of EVs-H on H/R injury in H9c2 cells. Inhibition of endogenous miR-208a and miR-208b restored QKI5 and QKI6 after H/R treatment. Dual-luciferase assay confirmed direct bindings between miR-208a/b and QKI 3'UTR. Functionally, QKI5 overexpression significantly suppressed H/R-induced CM apoptosis and suppressed the enhancing effect of EVs-H on CM apoptosis. Therefore, we infer that EVs-mediated transfer of miR-208a/b can exaggerate H/R injury in CMs by reducing QKI expression. This represents a previously unrecognized pathway of H/R injury in CMs.
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