ArticleAnnals of translational medicine2019
microRNA-1 inhibits cardiomyocyte proliferation in mouse neonatal hearts by repressing CCND1 expression.
Article in Annals of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Fibrosis suppressive effect and mechanism of CaSR positive allosteric modulators/p-dioxanone copolymers.Drug delivery and translational research · 2026Article
- Review
- MiRNA Regulations in Cardiotoxicity Induced by Oncologic Therapies and Possible Immune Response.Current medicinal chemistry · 2026Review
- Targeting miRNA-1a and miRNA-15b: A Novel Combinatorial Strategy to Drive Adult Cardiac Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Regulation of vascular smooth muscle cells phenotype by metformin up-regulated miR-1/ CCND1 axis via targeting AMPK/TGF-β signaling pathway.Molecular biology reports · 2025Article
- Rivaroxaban Ameliorates Sunitinib-Induced Injury of Cardiomyocytes via Repressing MAPK Signaling Pathway.Cardiovascular therapeutics · 2025Article
- Cardiac regeneration: Pre-existing cardiomyocyte as the hub of novel signaling pathway.Genes & diseases · 2024Review
- Space microgravity increases expression of genes associated with proliferation and differentiation in human cardiac spheres.NPJ microgravity · 2023Article
- miRNAs Epigenetic Tuning of Wall Remodeling in the Early Phase after Myocardial Infarction: A Novel Epidrug Approach.International journal of molecular sciences · 2023Review
- A change of heart: understanding the mechanisms regulating cardiac proliferation and metabolism before and after birth.The Journal of physiology · 2023Review
- Epigenetic Modification Factors and microRNAs Network Associated with Differentiation of Embryonic Stem Cells and Induced Pluripotent Stem Cells toward Cardiomyocytes: A Review.Life (Basel, Switzerland) · 2023Review
- Space microgravity improves proliferation of human iPSC-derived cardiomyocytes.Stem cell reports · 2022Article
- Heart regeneration: 20 years of progress and renewed optimism.Developmental cell · 2022Review
- Restoring Ravaged Heart: Molecular Mechanisms and Clinical Application of miRNA in Heart Regeneration.Frontiers in cardiovascular medicine · 2022Review
- miRNA in cardiac development and regeneration.Cell regeneration (London, England) · 2021Review
- Differential Spatio-Temporal Regulation of T-Box Gene Expression by microRNAs during Cardiac Development.Journal of cardiovascular development and disease · 2021Article
- Non-coding RNA Regulated Cross-Talk Between Mitochondria and Other Cellular Compartments.Frontiers in cell and developmental biology · 2021Review
- Arteriovenous Fistula-induced Cardiac Remodeling Shows Cardioprotective Features in Mice.JVS-vascular science · 2021Article
- Non-coding RNAs: emerging players in cardiomyocyte proliferation and cardiac regeneration.Basic research in cardiology · 2020Review
- Identification and validation of hub microRNAs dysregulated in esophageal squamous cell carcinoma.Aging · 2020Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe functions of microRNA-1 (miR-1) in cardiac hypertrophy, and cardiomyocyte differentiation have been investigated. However, the mechanism on how miR-1 could repress cardiomyocyte proliferation has not been fully elucidated.
methodsWe address this issue by investigating whether miR-1 affected the proliferation of neonatal cardiomyocyte and identify some of the genes targeted by miR-1. miR-1 was over-expressed in neonatal cardiomyocytes and the effect on cell cycle and growth were analyzed by flow cytometry and Brdu-incorporation assay. Relevant vectors carrying the luciferase reporter were constructed for validation of miR-1 binding to its matching sites on the 3'-untranslated region of the predicated target mRNAs. Cardiomyocytes were co-transfected with the vectors and miR-1 mimics, then luciferase reporter assay was performed. Lastly, we examined the expression of target genes in cardiomyocytes after transfection with miR-1 mimics, as well as their normal expression pattern in 2- and 13-day-old mice hearts.
resultsWe have demonstrated that miR-1 was the most significantly upregulated miRNA in 13-day-old mouse hearts compared with 2-day-old hearts. We also showed that miR-1 could repress cardiomyocyte G1/S phase transition, proliferation and viability. IGF1 and CCND1 were identified as candidate target genes regulated by miR-1. In addition, overexpression of miR-1 could suppress the expression of these two genes at the mRNA level. It could also correspondingly inhibit CCND1 expression at the protein level but not for IGF1.
conclusionsOur results suggest that miR-1 plays an important role in inhibiting cardiomyocyte proliferation in the developing neonatal mouse heart by directly suppressing the cell-cycle regulator, CCND1.
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