ArticleNucleic acids research2021
Novel roles of an intragenic G-quadruplex in controlling microRNA expression and cardiac function.
Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- Three- and four-stranded nucleic acid structures and their ligands.RSC chemical biology · 2025Review
- Apurinic/Apyrimidinic Endodeoxyribonuclease 1 modulates RNA G-quadruplex folding of miR-92b and controls its expression in cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- SingmiR: a single-cell miRNA alignment and analysis tool.Nucleic acids research · 2024Article
- FAM3A Deficiency - Induced Mitochondrial Dysfunction Underlies Post-Infarct Mortality and Heart Failure.Journal of cardiovascular translational research · 2024Article
- Extracellular Vesicle MicroRNAs in Heart Failure: Pathophysiological Mediators and Therapeutic Targets.Cells · 2023Review
- Dynamic alternative DNA structures in biology and disease.Nature reviews. Genetics · 2023Review
- G-Quadruplexes Regulate miRNA Biogenesis in Live Zebrafish Embryos.International journal of molecular sciences · 2023Article
- Wild emmer wheat, the progenitor of modern bread wheat, exhibits great diversity in theFrontiers in plant science · 2022Article
- Ligands as Stabilizers of G-Quadruplexes in Non-Coding RNAs.Molecules (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
20 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Simultaneous dysregulation of multiple microRNAs (miRs) affects various pathological pathways related to cardiac failure. In addition to being potential cardiac disease-specific markers, miR-23b/27b/24-1 were reported to be responsible for conferring cardiac pathophysiological processes. In this study, we identified a conserved guanine-rich RNA motif within the miR-23b/27b/24-1 cluster that can form an RNA G-quadruplex (rG4) in vitro and in cells. Disruption of this intragenic rG4 significantly increased the production of all three miRs. Conversely, a G4-binding ligand tetrandrine (TET) stabilized the rG4 and suppressed miRs production in human and rodent cardiomyocytes. Our further study showed that the rG4 prevented Drosha-DGCR8 binding and processing of the pri-miR, suppressing the biogenesis of all three miRs. Moreover, CRISPR/Cas9-mediated G4 deletion in the rat genome aberrantly elevated all three miRs in the heart in vivo, leading to cardiac contractile dysfunction. Importantly, loss of the G4 resulted in reduced targets for the aforementioned miRs critical for normal heart function and defects in the L-type Ca2+ channel-ryanodine receptor (LCC-RyR) coupling in cardiomyocytes. Our results reveal a novel mechanism for G4-dependent regulation of miR biogenesis, which is essential for maintaining normal heart function.
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