Upregulation of miRNA-23a-3p rescues high glucose-induced cell apoptosis and proliferation inhibition in cardiomyocytes
Open accessAbstract
Maternal hyperglycemia potentially inhibits the development of the fetal heart by suppressing cardiomyocyte proliferation and promoting apoptosis. Different studies have indicated that miRNAs are key regulators of cardiomyocyte proliferation, differentiation, and apoptosis and play a protective role in a variety of cardiovascular diseases. However, the biological function of miRNA-23a in hyperglycemia-related cardiomyocyte injury is not fully understood. The present study investigated the effect of miRNA-23a-3p on cell proliferation and apoptosis in a myocardial injury model induced by high glucose. H9c2 cardiomyocytes were exposed to high glucose to establish an in vitro myocardial injury model and then transfected with miRNA-23a-3p mimics. After miRNA-23a-3p transfection, lens-free microscopy was used to dynamically monitor cell numbers and confluence and calculate the cell cycle duration. CCK-8 and EdU incorporation assays were performed to detect cell proliferation. Flow cytometry was used to measured cell apoptosis. Upregulation of miRNA-23a-3p significantly alleviated high glucose-induced cell apoptosis and cell proliferation inhibition (p < 0.01 and p < 0.0001, respectively). The cell cycle of the miRNA-23a-3p mimics group was significantly shorter than that of the negative control group (p < 0.01). The expression of cell cycle–activating and apoptosis inhibition-associated factors Ccna2, Ccne1, and Bcl-2 was downregulated by high glucose and upregulated by miRNA-23a-3p overexpression in high glucose-injured H9c2 cells. miRNA-23a-3p mimics transfection before high glucose treatment had a significantly greater benefit than transfection after high glucose treatment (p < 0.0001), and the rescue effect of miRNA-23a-3p increased as the concentration increased. This study suggests that miRNA-23a-3p exerted a dose- and time-dependent protective effect on high glucose-induced H9c2 cardiomyocyte injury.
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miRNA-23a-3p has a dose-dependent and time-dependent protective effect against high glucose-induced H9c2 cardiomyocyte injury.
“It was also discovered that miRNA-23a-3p has a dose-dependent and time-dependent protective effect against high glucose-induced H9c2 cardiomyocyte injury [59].”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [59]
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Functional screening identifies miRNAs inducing cardiac regeneration
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Liu, L., Cheng, Z., & Yang, J. (2018) · Pathology - Research and Practice · doi:10.1016/j.prp.2018.09.004 · Cited by 28 · see citing works
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Recent advances of miR-23 in human diseases and growth development
Qian, X., Jiang, Y., Yang, Y., Zhang, Y., Xu, N., Xu, B., Pei, K., Yu, Z., & Wu, W. (2025) · Non-coding RNA Research · doi:10.1016/j.ncrna.2024.12.010 · Cited by 5 · see citing works
Self-citation
- Authors
- Wu, F., Wang, F., Yang, Q., Zhang, Y., Cai, K., Liu, L., Li, S., Zheng, Y., Zhang, J., Gui, Y., Wang, Y., Wang, X., Gui, Y., & Li, Q.
- Affiliations
- Shanghai Jiao Tong University (CN)
- Fudan University (CN)
- Children's Hospital of Fudan University (CN)
- Shanghai University of Traditional Chinese Medicine (CN)
- Corresponding author
- Gui, Yiting
- Gui, Yonghao
- Li, Qiang
- ORCID
- Venue
- In Vitro Cellular & Developmental Biology - Animal
- Published
- 2020-11-16
- Volume
- 56
- Issue
- 10
- Pages
- 866-877
- ISSN
- 1071-2690 (ISSN-L)
- 1543-706X
- PMC
- PMC7723946
- OpenAlex
- W3105762711
- Cited by
- 28
- References
- 2
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 3 · 2023: 3 · 2022: 11 · 2021: 5
- FWCI
- 1.54
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- In Vitro Cellular & Developmental Biology - Animal (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81470442, 81873481, 2016YFC1000500, 81771632)
- National Key Research and Development Program of China (2016YFC1000500)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Keywords
- high glucose, cardiomyocyte apoptosis, cardiomyocyte proliferation, myocardial injury, maternal hyperglycemia, fetal heart development, cell cycle, cyclin A2, cyclin E1, Bcl-2, H9c2 cells
- MeSH terms
- Animals, Cell Line, Glucose, Up-Regulation, Apoptosis, Myocytes, Cardiac, MicroRNAs, Cell Proliferation, Rats
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