ArticleNucleic acids research2014
The primary microRNA-208b interacts with Polycomb-group protein, Ezh2, to regulate gene expression in the heart.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 68 citations in OpenAlex.
- The paradox of nuclear miRNAs: Mechanisms, therapeutic potential, and future directions.Non-coding RNA research · 2026Review
- Integrated analysis of MYH6, MYH7, and MYH7B expression and their associated microRNAs in human end-stage heart failure.Frontiers in cardiovascular medicine · 2026Article
- Unraveling the relevance of SARS-Cov-2 infection and ferroptosis within the heart of COVID-19 patients.Heliyon · 2024Article
- Nuclear miRNAs: Gene Regulation Activities.International journal of molecular sciences · 2024Review
- Chromatin modifiers in human disease: from functional roles to regulatory mechanisms.Molecular biomedicine · 2024Review
- Noncanonical functions of microRNAs in the nucleus.Acta biochimica et biophysica Sinica · 2024Review
- Ferroptosis contributes to ethanol-induced hepatic cell death via labile iron accumulation and GPx4 inactivation.Cell death discovery · 2023Article
- Targeting Epigenetic Regulation of Cardiomyocytes through Development for Therapeutic Cardiac Regeneration after Heart Failure.International journal of molecular sciences · 2022Review
- Non-canonical features of microRNAs: paradigms emerging from cardiovascular disease.Nature reviews. Cardiology · 2022Review
- Mechanism of histone deacetylases in cardiac hypertrophy and its therapeutic inhibitors.Frontiers in cardiovascular medicine · 2022Review
- Knockdown of long noncoding RNA GAS5 reduces vascular smooth muscle cell apoptosis by inactivating EZH2-mediated RIG-I signaling pathway in abdominal aortic aneurysm.Journal of translational medicine · 2021Article
- The role and molecular mechanism of epigenetics in cardiac hypertrophy.Heart failure reviews · 2021Review
- Histone Acetylation Domains Are Differentially Induced during Development of Heart Failure in Dahl Salt-Sensitive Rats.International journal of molecular sciences · 2021Article
- Targeting muscle-enriched long non-coding RNA H19 reverses pathological cardiac hypertrophy.European heart journal · 2020Article
- MicroRNA-26a Protects the Heart Against Hypertension-Induced Myocardial Fibrosis.Journal of the American Heart Association · 2020Article
- Regulation of myosin heavy chain antisense long noncoding RNA in human vastus lateralis in response to exercise training.American journal of physiology. Cell physiology · 2020Article
- Functional Dissection of pri-miR-290~295 in Dgcr8 Knockout Mouse Embryonic Stem Cells.International journal of molecular sciences · 2019Article
- Sex-Based Mhrt Methylation Chromatinizes MeCP2 in the Heart.iScience · 2019Article
- Mitochondrial proteome disruption in the diabetic heart through targeted epigenetic regulation at the mitochondrial heat shock protein 70 (mtHsp70) nuclear locus.Journal of molecular and cellular cardiology · 2018Article
- Epigenomes in Cardiovascular Disease.Circulation research · 2018Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Polycomb-group protein, Ezh2, is required for epigenetic gene silencing in the adult heart by unknown mechanism. We investigated the role of Ezh2 and non-coding RNAs in a mouse model of pressure overload using transverse aortic constriction (TAC) attenuated by the prototypical histone deacetylase inhibitor, trichostatin A (TSA). Chromatin immunoprecipitation of TAC and TAC+TSA hearts suggests interaction of Ezh2 and primary microRNA-208b (pri-miR-208b) in the regulation of hypertrophic gene expression. RNAi silencing of pri-miR-208b and Ezh2 validate pri-miR-208b-mediated transcriptional silencing of genes implicated in cardiac hypertrophy including the suppression of the bi-directional promoter (bdP) of the cardiac myosin heavy chain genes. In TAC mouse heart, TSA attenuated Ezh2 binding to bdP and restored antisense β-MHC and α-MHC gene expression. RNA-chromatin immunoprecipitation experiments in TAC hearts also show increased pri-miR-208b dependent-chromatin binding. These results are the first description by which primary miR interactions serve to integrate chromatin modifications and the transcriptional response to distinct signaling cues in the heart. These studies provide a framework for MHC expression and regulation of genes implicated in pathological remodeling of ventricular hypertrophy.
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