ArticleInternational journal of molecular sciences2015
miR-134 Modulates the Proliferation of Human Cardiomyocyte Progenitor Cells by Targeting Meis2.
Article in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Distinct microRNA profiles in neuron-derived extracellular vesicles between recent-onset and chronic-phase schizophrenia.Schizophrenia (Heidelberg, Germany) · 2025Article
- Promoter-targeted small RNA duplexes increase MBNL1 transcription and mitigate myotonic dystrophy-associated spliceopathy.Nucleic acids research · 2025Article
- LncRNAs in theInternational journal of molecular sciences · 2024Article
- microRNA and the Post-Transcriptional Response to Oxidative Stress during Neuronal Differentiation: Implications for Neurodevelopmental and Psychiatric Disorders.Life (Basel, Switzerland) · 2024Article
- Identification and validation of aging-related genes in heart failure based on multiple machine learning algorithms.Frontiers in immunology · 2024Article
- 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
- Review
- NcRNAs in Vascular and Valvular Intercellular Communication.Frontiers in molecular biosciences · 2021Review
- The microRNA miR-134-5p induces calcium deposition by inhibiting histone deacetylase 5 in vascular smooth muscle cells.Journal of cellular and molecular medicine · 2020Article
- Neural crest cells require Meis2 for patterning the mandibular arch via the Sonic hedgehog pathway.Biology open · 2020Article
- Circulating MicroRNAs: Biogenesis and Clinical Significance in Acute Myocardial Infarction.Frontiers in physiology · 2020Review
- MicroRNA-134-5p Regulates Media Degeneration through Inhibiting VSMC Phenotypic Switch and Migration in Thoracic Aortic Dissection.Molecular therapy. Nucleic acids · 2019Article
- MiRNA-134 suppresses esophageal squamous cell carcinoma progression by targeting FOXM1.International journal of clinical and experimental pathology · 2019Article
- Effect of miR-134 against myocardial hypoxia/reoxygenation injury by directly targeting NOS3 and regulating PI3K/Akt pathway.Acta cirurgica brasileira · 2019Article
- Maturation of Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes by Soluble Factors from Human Mesenchymal Stem Cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2018Article
- A Hearty Dose of Noncoding RNAs: The ImprintedJournal of cardiovascular development and disease · 2018Review
- Prospective and therapeutic screening value of non-coding RNA as biomarkers in cardiovascular disease.Annals of translational medicine · 2016Review
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiomyocyte progenitor cells play essential roles in early heart development, which requires highly controlled cellular organization. microRNAs (miRs) are involved in various cell behaviors by post-transcriptional regulation of target genes. However, the roles of miRNAs in human cardiomyocyte progenitor cells (hCMPCs) remain to be elucidated. Our previous study showed that miR-134 was significantly downregulated in heart tissue suffering from congenital heart disease, underlying the potential role of miR-134 in cardiogenesis. In the present work, we showed that the upregulation of miR-134 reduced the proliferation of hCMPCs, as determined by EdU assay and Ki-67 immunostaining, while the inhibition of miR-134 exhibited an opposite effect. Both up- and downregulation of miR-134 expression altered the transcriptional level of cell-cycle genes. We identified Meis2 as the target of miR-134 in the regulation of hCMPC proliferation through bioinformatic prediction, luciferase reporter assay and western blot. The over-expression of Meis2 mitigated the effect of miR-134 on hCMPC proliferation. Moreover, miR-134 did not change the degree of hCMPC differentiation into cardiomyocytes in our model, suggesting that miR-134 is not required in this process. These findings reveal an essential role for miR-134 in cardiomyocyte progenitor cell biology and provide new insights into the physiology and pathology of cardiogenesis.
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