ArticleStem cells international2015
Inhibition of G9a Histone Methyltransferase Converts Bone Marrow Mesenchymal Stem Cells to Cardiac Competent Progenitors.
Article in Stem cells international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Stem Cells Associated with Adult Skeletal Muscle Can Form Beating Cardiac Tissue In Vitro in Response to Media Containing Heparin, Dexamethasone, Growth Factors and Hydrogen Peroxide.International journal of molecular sciences · 2025Article
- Inhibition of histone methyltransferase G9a promotes the osteogenic potential of bone-derived stem cells in diabetic-osteoporosis by regulating the LINC00657/miR-204-5p/IGFBP5 pathway.Frontiers in endocrinology · 2025Article
- G9a inhibition promotes the formation of pacemaker-like cells by reducing the enrichment of H3K9me2 in the HCN4 promoter region.Molecular medicine reports · 2023Article
- Chromatin-modifying drugs and metabolites in cell fate control.Cell proliferation · 2020Review
- The combination of G9a histone methyltransferase inhibitors with erythropoietin protects heart against damage from acute myocardial infarction.American journal of translational research · 2020Article
- Article
- Long noncoding RNA Braveheart promotes cardiogenic differentiation of mesenchymal stem cells in vitro.Stem cell research & therapy · 2017Article
- Inhibition of Histone Methyltransferase, Histone Deacetylase, andStem cells international · 2017Article
- BIX01294, an inhibitor of histone methyltransferase, induces autophagy-dependent differentiation of glioma stem-like cells.Scientific reports · 2016Article
- Mesenchymal stem cells in cardiac regeneration: a detailed progress report of the last 6 years (2010-2015).Stem cell research & therapy · 2016Review
- G9a histone methyltransferase inhibitor BIX01294 promotes expansion of adult cardiac progenitor cells without changing their phenotype or differentiation potential.Cell proliferation · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The G9a histone methyltransferase inhibitor BIX01294 was examined for its ability to expand the cardiac capacity of bone marrow cells. Inhibition of G9a histone methyltransferase by gene specific knockdown or BIX01294 treatment was sufficient to induce expression of precardiac markers Mesp1 and brachyury in bone marrow cells. BIX01294 treatment also allowed bone marrow mesenchymal stem cells (MSCs) to express the cardiac transcription factors Nkx2.5, GATA4, and myocardin when subsequently exposed to the cardiogenic stimulating factor Wnt11. Incubation of BIX01294-treated MSCs with cardiac conditioned media provoked formation of phase bright cells that exhibited a morphology and molecular profile resembling similar cells that normally form from cultured atrial tissue. Subsequent aggregation and differentiation of BIX01294-induced, MSC-derived phase bright cells provoked their cardiomyogenesis. This latter outcome was indicated by their widespread expression of the primary sarcomeric proteins muscle α-actinin and titin. MSC-derived cultures that were not initially treated with BIX01294 exhibited neither a commensurate burst of phase bright cells nor stimulation of sarcomeric protein expression. Collectively, these data indicate that BIX01294 has utility as a pharmacological agent that could enhance the ability of an abundant and accessible stem cell population to regenerate new myocytes for cardiac repair.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.