ArticleThe Journal of biological chemistry2011
Myocyte enhancer factor-2 interacting transcriptional repressor (MITR) is a switch that promotes osteogenesis and inhibits adipogenesis of mesenchymal stem cells by inactivating peroxisome proliferator-activated receptor gamma-2.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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33 citing papers in PubMed, 59 citations in OpenAlex.
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- Synthesis and biological evaluation ofJournal of enzyme inhibition and medicinal chemistry · 2024Article
- Histone deacetylase (HDAC) 9: versatile biological functions and emerging roles in human cancer.Cellular oncology (Dordrecht, Netherlands) · 2021Review
- The PPARα and PPARγ Epigenetic Landscape in Cancer and Immune and Metabolic Disorders.International journal of molecular sciences · 2021Review
- Combination of BMP2 and EZH2 Inhibition to Stimulate Osteogenesis in a 3D Bone Reconstruction Model.Tissue engineering. Part A · 2021Article
- Quis Custodiet Ipsos Custodes (Who Controls the Controllers)? Two Decades of Studies on HDAC9.Life (Basel, Switzerland) · 2021Review
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- Non-Coding RNAs Steering the Senescence-Related Progress, Properties, and Application of Mesenchymal Stem Cells.Frontiers in cell and developmental biology · 2021Review
- Histone Deacetylase 9: Its Role in the Pathogenesis of Diabetes and Other Chronic Diseases.Diabetes & metabolism journal · 2020Review
- A preview of selected articles.Stem cells translational medicine · 2020Review
- FOXM1 drives proximal tubule proliferation during repair from acute ischemic kidney injury.The Journal of clinical investigation · 2019Article
- Sodium Selenite Improves The Therapeutic Effect Of BMSCs Via Promoting The Proliferation And Differentiation, Thereby Promoting The Hematopoietic Factors.OncoTargets and therapy · 2019Article
- Enhancer of zeste homolog 2 (The Journal of biological chemistry · 2018Article
- Mutual inhibition between HDAC9 and miR-17 regulates osteogenesis of human periodontal ligament stem cells in inflammatory conditions.Cell death & disease · 2018Article
- Bone Marrow Fat and Hematopoiesis.Frontiers in endocrinology · 2018Review
- YY1 and HDAC9c transcriptionally regulate p38-mediated mesenchymal stem cell differentiation into osteoblasts.American journal of cancer research · 2018Article
- ARN: Analysis and Visualization System for Adipogenic Regulation Network Information.Scientific reports · 2016Article
- ARN: analysis and prediction by adipogenic professional database.BMC systems biology · 2016Article
- RECK (reversion-inducing cysteine-rich protein with Kazal motifs) regulates migration, differentiation and Wnt/β-catenin signaling in human mesenchymal stem cells.Cellular and molecular life sciences : CMLS · 2016Article
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
EZH2, a catalytic subunit of Polycomb-repressive complex 2 (PRC2), is a histone lysine methyltransferase that methylates lysine 27 of histone H3, resulting in gene silencing. It has been shown that EZH2 plays a pivotal role in fostering self-renewal and inhibiting the differentiation of embryonic stem cells. Mesenchymal stem cells (MSCs) can be induced to differentiate into adipogenic and osteogenic lineages, which are mutually exclusive. However, it is not clear whether the molecular events of EZH2-mediated epigenetic silencing may coordinate differentiation between osteoblasts and adipocytes. Disruption of the balance between adipogenesis and osteogenesis is associated with many diseases; thus, identifying a switch that determines the fate of MSC is critical. In this study, we used EZH2-ChIP-on-chip assay to identify differential EZH2 targets in the two differentiation stages on a genome-wide scale. After validating the targets, we found that myocyte enhancer factor-2 interacting transcriptional repressor (MITR)/HDAC9c was expressed in osteoblasts and greatly decreased in adipocytes. We demonstrated that MITR plays a crucial role in the acceleration of MSC osteogenesis and attenuation of MSC adipogenesis through interaction with peroxisome proliferator-activated receptor (PPAR) γ-2 in the nucleus of osteoblasts, which interrupts PPARγ-2 activity and prevents adipogenesis. Together, our results demonstrated that MITR plays a master switch role to balance osteogenic and adipogenic differentiation of MSCs through regulation of PPARγ-2 transcriptional activity.
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