ArticleScientific reports2016
Btg2 is a Negative Regulator of Cardiomyocyte Hypertrophy through a Decrease in Cytosolic RNA.
Article in Scientific reports, 2016. 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, 28 citations in OpenAlex.
- Research progress on BTG2 in non‑tumor diseases (Review).International journal of molecular medicine · 2026Review
- Integrated bioinformatics and clinical validation of oxidative stress-associated genes in atrial fibrillation and chronic kidney disease.Experimental and therapeutic medicine · 2026Article
- Diagnostic potential of B-cell translocation gene 2 in IgA nephropathy: Insights from molecular mechanisms.Journal of cell communication and signaling · 2026Article
- Silicate biomaterials-based multicellular scaffolds with specific cellular spatial distribution for infarcted myocardium repair.Bioactive materials · 2026Article
- Identification of a key smooth muscle cell subset driving ischemic cardiomyopathy progression through single-cell RNA sequencing.Scientific reports · 2025Article
- Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by spatial and single-cell transcriptomics.Science advances · 2025Article
- Modeling cardiomyocyte signaling and metabolism predicts genotype-to-phenotype mechanisms in hypertrophic cardiomyopathy.Computers in biology and medicine · 2024Article
- Btg1 and Btg2 regulate neonatal cardiomyocyte cell cycle arrest.Journal of molecular and cellular cardiology · 2023Article
- Human-Induced Pluripotent Stem Cell-Derived Cardiomyocyte Model forCirculation. Genomic and precision medicine · 2022Article
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- Cardiac-specific microRNA-125b deficiency induces perinatal death and cardiac hypertrophy.Scientific reports · 2021Article
- Adeno-associated virus-mediated gene delivery promotes S-phase entry-independent precise targeted integration in cardiomyocytes.Scientific reports · 2020Article
- Metabolic Remodeling Promotes Cardiac Hypertrophy by Directing Glucose to Aspartate Biosynthesis.Circulation research · 2020Article
- Transcriptome analysis defines myocardium gene signatures in children with ToF and ASD and reveals disease-specific molecular reprogramming in response to surgery with cardiopulmonary bypass.Journal of translational medicine · 2020Article
- The impact of in vitro cell culture duration on the maturation of human cardiomyocytes derived from induced pluripotent stem cells of myogenic origin.Cell transplantation · 2018Article
- Targeted Genome Replacement via Homology-directed Repair in Non-dividing Cardiomyocytes.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Under hypertrophic stimulation, cardiomyocytes enter a hypermetabolic state and accelerate biomass accumulation. Although the molecular pathways that regulate protein levels are well-studied, the functional implications of RNA accumulation and its regulatory mechanisms in cardiomyocytes remain elusive. Here, we have elucidated the quantitative kinetics of RNA in cardiomyocytes through single cell imaging and c-Myc (Myc)-mediated hypermetabolic analytical model using cultured cardiomyocytes. Nascent RNA labeling combined with single cell imaging demonstrated that Myc protein significantly increased the amount of global RNA production per cardiomyocyte. Chromatin immunoprecipitation with high-throughput sequencing clarified that overexpressed Myc bound to a specific set of genes and recruits RNA polymerase II. Among these genes, we identified Btg2 as a novel target of Myc. Btg2 overexpression significantly reduced cardiomyocyte surface area. Conversely, shRNA-mediated knockdown of Btg2 accelerated adrenergic stimulus-induced hypertrophy. Using mass spectrometry analysis, we determined that Btg2 binds a series of proteins that comprise mRNA deadenylation complexes. Intriguingly, Btg2 specifically suppresses cytosolic, but not nuclear, RNA levels. Btg2 knockdown further enhances cytosolic RNA accumulation in cardiomyocytes under adrenergic stimulation, suggesting that Btg2 negatively regulates reactive hypertrophy by negatively regulating RNA accumulation. Our findings provide insight into the functional significance of the mechanisms regulating RNA levels in cardiomyocytes.
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