ArticleThe Journal of biological chemistry2015
Epigenetic Control of Skeletal Development by the Histone Methyltransferase Ezh2.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.
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Who cites it
110 citing papers in PubMed, 177 citations in OpenAlex.
- Epigenetic regulation of vertebrate limb development: from field specification to tissue morphogenesis.Epigenetics · 2026Review
- Inhibition of EED enhances osteogenic differentiation and bone formation: a potential therapeutic strategy for osteogenesis imperfecta.JBMR plus · 2026Article
- Engineering Extracellular Vesicle Production Through Magnetic Ion Channel Activation for Bone Regeneration.Advanced healthcare materials · 2026Article
- Behavioral and transcriptomic markers of susceptibility to escalate fentanyl intake.Translational psychiatry · 2026Article
- Enhancer of zeste homolog 2 (Ezh2) is required in mouse Isl1-expressing progenitors for proper development of cardiac and skeletal hindlimb structures.Biology open · 2026Article
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- CXXC Finger Protein 1 drives BMP signaling and progenitor cell differentiation during limb development.Developmental biology · 2025Article
- Revealing the biophysics of lamina-associated domain formation by integrating theoretical modeling and high-resolution imaging.Nature communications · 2025Article
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- Epigenetic Control of Osteogenesis: Pathways Toward Improved Bone Regeneration.Current osteoporosis reports · 2025Review
- Inhibition of KDM6B prevents osteoarthritis by blocking growth plate-like H3K27me3 loss in bivalent genes.Science China. Life sciences · 2025Article
- Role and mechanisms of histone methylation in osteogenic/odontogenic differentiation of dental mesenchymal stem cells.International journal of oral science · 2025Review
- RNA Sequencing Revealed a Weak Response of Gingival Fibroblasts Exposed to Hyaluronic Acid.Bioengineering (Basel, Switzerland) · 2024Article
- Dynamic strain and β-catenin mediated suppression of interferon responsive genes in quiescent mesenchymal stromal/stem cells.Biochemistry and biophysics reports · 2024Article
- Mesenchymal Wnts are required for morphogenetic movements of calvarial osteoblasts during apical expansion.Development (Cambridge, England) · 2024Article
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- Exploring epigenetic strategies for the treatment of osteoporosis.Molecular biology reports · 2024Review
- AdipoRon reduces TGFβ1-mediated collagen deposition in vitro and alleviates knee stiffness in vivo.Journal of cellular physiology · 2024Article
- A Germinal Center Checkpoint of AIRE in B Cells Limits Antibody Diversification.bioRxiv : the preprint server for biology · 2024Article
50 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 5 institutions in 3 countries.
Funding
Abstract
Epigenetic control of gene expression is critical for normal fetal development. However, chromatin-related mechanisms that activate bone-specific programs during osteogenesis have remained underexplored. Therefore, we investigated the expression profiles of a large cohort of epigenetic regulators (>300) during osteogenic differentiation of human mesenchymal cells derived from the stromal vascular fraction of adipose tissue (AMSCs). Molecular analyses establish that the polycomb group protein EZH2 (enhancer of zeste homolog 2) is down-regulated during osteoblastic differentiation of AMSCs. Chemical inhibitor and siRNA knockdown studies show that EZH2, a histone methyltransferase that catalyzes trimethylation of histone 3 lysine 27 (H3K27me3), suppresses osteogenic differentiation. Blocking EZH2 activity promotes osteoblast differentiation and suppresses adipogenic differentiation of AMSCs. High throughput RNA sequence (mRNASeq) analysis reveals that EZH2 inhibition stimulates cell cycle inhibitory proteins and enhances the production of extracellular matrix proteins. Conditional genetic loss of Ezh2 in uncommitted mesenchymal cells (Prrx1-Cre) results in multiple defects in skeletal patterning and bone formation, including shortened forelimbs, craniosynostosis, and clinodactyly. Histological analysis and mRNASeq profiling suggest that these effects are attributable to growth plate abnormalities and premature cranial suture closure because of precocious maturation of osteoblasts. We conclude that the epigenetic activity of EZH2 is required for skeletal patterning and development, but EZH2 expression declines during terminal osteoblast differentiation and matrix production.
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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.