ArticleInternational journal of biological sciences2015
MicroRNA-23a participates in estrogen deficiency induced gap junction remodeling of rats by targeting GJA1.
Article in International journal of biological sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 27 citations in OpenAlex.
- Epigenetic regulation of electromechanical continuity might determine phenotypic heterogeneity in SCN5A mutation carriers in Brugada syndrome.Scientific reports · 2025Article
- Bazi Bushen capsule attenuates cardiac systolic injury via SIRT3/SOD2 pathway in high-fat diet-fed ovariectomized mice.Heliyon · 2024Article
- AhR/miR-23a-3p/PKCα axis contributes to memory deficits in ovariectomized and normal aging female mice.Molecular therapy. Nucleic acids · 2021Article
- Approaching Sex Differences in Cardiovascular Non-Coding RNA Research.International journal of molecular sciences · 2020Review
- Connecting sex differences, estrogen signaling, and microRNAs in cardiac fibrosis.Journal of molecular medicine (Berlin, Germany) · 2019Review
- microRNA and Other Small RNA Sequence Profiling across Six Tissues of Chinese Forest Musk Deer (BioMed research international · 2019Article
- miRNA as a New Regulatory Mechanism of Estrogen Vascular Action.International journal of molecular sciences · 2018Review
- Role of miRNA in the Regulatory Mechanisms of Estrogens in Cardiovascular Ageing.Oxidative medicine and cellular longevity · 2018Review
- Connexins in Cardiovascular and Neurovascular Health and Disease: Pharmacological Implications.Pharmacological reviews · 2017Review
- Article
- MicroRNA-19b Downregulates Gap Junction Protein Alpha1 and Synergizes with MicroRNA-1 in Viral Myocarditis.International journal of molecular sciences · 2016Article
- Expression of the Mir-133 and Bcl-2 could be affected by swimming training in the heart of ovariectomized rats.Iranian journal of basic medical sciences · 2016Article
- Methylation Status of SP1 Sites within miR-23a-27a-24-2 Promoter Region Influences Laryngeal Cancer Cell Proliferation and Apoptosis.BioMed research international · 2016Article
- Regulation of Connexins Expression Levels by MicroRNAs, an Update.Frontiers in physiology · 2016Review
- EFFECTS OF EXERCISE ON MIR-29 AND IGF-1 EXPRESSION AND LIPID PROFILE IN THE HEART OF OVARIECTOMIZED RAT.Acta endocrinologica (Bucharest, Romania : 2005)Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increased incidence of arrhythmias in women after menopause has been widely documented, which is considered to be related to estrogen (E2) deficiency induced cardiac electrophysiological abnormalities. However, its molecular mechanism remains incompletely clear. In the present study, we found cardiac conduction blockage in post-menopausal rats. Thereafter, the results showed that cardiac gap junctions were impaired and Connexin43 (Cx43) expression was reduced in the myocardium of post-menopausal rats. The phenomenon was also observed in ovariectomized (OVX) rats, which was attenuated by E2 supplement. Further study displayed that microRNA-23a (miR-23a) level was significantly increased in both post-menopausal and OVX rats, which was reversed by daily E2 treatment after OVX. Importantly, forced overexpression of miR-23a led to gap junction impairment and Cx43 downregulation in cultured cardiomyocytes, which was rescued by suppressing miR-23a by transfection of miR-23a specific inhibitory oligonucleotide (AMO-23a). GJA1 was identified as the target gene of miR-23a by luciferase assay and miRNA-masking antisense ODN (miR-Mask) assay. We also found that E2 supplement could reverse cardiac conduction blockage, Cx43 downregulation, gap junction remodeling and miR-23a upregulation in post-menopausal rats. These findings provide the evidence that miR-23a mediated repression of Cx43 participates in estrogen deficiency induced damages of cardiac gap junction, and highlights a new insight into molecular mechanism of post-menopause related arrhythmia at the microRNA level.
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