ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2017
Histone Deacetylase 3 Deletion in Mesenchymal Progenitor Cells Hinders Long Bone Development.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- Investigating the Differential Circulating microRNA Expression in Adolescent Females with Severe Idiopathic Scoliosis: A Proof-of-Concept Observational Clinical Study.International journal of molecular sciences · 2024Observational
- The Role of the Kynurenine Pathway in the Pathophysiology of Frailty, Sarcopenia, and Osteoporosis.Nutrients · 2023Review
- Epigenetic control of mesenchymal stem cells orchestrates bone regeneration.Frontiers in endocrinology · 2023Review
- Histone deacetylase 3 (HDAC3) as an important epigenetic regulator of kidney diseases.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Article
- Article
- The Role of Histone Deacetylase 3 Complex in Nuclear Hormone Receptor Action.International journal of molecular sciences · 2021Review
- Single-Cell Atlas Reveals Fatty Acid Metabolites Regulate the Functional Heterogeneity of Mesenchymal Stem Cells.Frontiers in cell and developmental biology · 2021Article
- The Role of Fibroblast Growth Factor 21 in Diabetic Cardiovascular Complications and Related Epigenetic Mechanisms.Frontiers in endocrinology · 2021Review
- Hdac3 regulates bone modeling by suppressing osteoclast responsiveness to RANKL.The Journal of biological chemistry · 2020Article
- Review
- Epigenetic Therapies for Osteoarthritis.Trends in pharmacological sciences · 2020Review
- Epigenetic Regulation of Skeletal Tissue Integrity and Osteoporosis Development.International journal of molecular sciences · 2020Review
- Age-related increase of kynurenine enhances miR29b-1-5p to decrease both CXCL12 signaling and the epigenetic enzyme Hdac3 in bone marrow stromal cells.Bone reports · 2020Article
- Interplay between genetics and epigenetics in osteoarthritis.Nature reviews. Rheumatology · 2020Review
- Coordinated expression of p300 and HDAC3 upregulates histone acetylation during dentinogenesis.Journal of cellular biochemistry · 2020Article
- Control of mesenchymal stem cell biology by histone modifications.Cell & bioscience · 2020Review
- Concise Review: The Regulatory Mechanism of Lysine Acetylation in Mesenchymal Stem Cell Differentiation.Stem cells international · 2020Review
- Bone Remodeling: Histone Modifications as Fate Determinants of Bone Cell Differentiation.International journal of molecular sciences · 2019Review
- Hepatic Osteodystrophy-Molecular Mechanisms Proposed to Favor Its Development.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Long bone formation is a complex process that requires precise transcriptional control of gene expression programs in mesenchymal progenitor cells. Histone deacetylases (Hdacs) coordinate chromatin structure and gene expression by enzymatically removing acetyl groups from histones and other proteins. Hdac inhibitors are used clinically to manage mood disorders, cancers, and other conditions but are teratogenic to the developing skeleton and increase fracture risk in adults. In this study, the functions of Hdac3, one of the enzymes blocked by current Hdac inhibitor therapies, in skeletal mesenchymal progenitor cells were determined. Homozygous deletion of Hdac3 in Prrx1-expressing cells prevented limb lengthening, altered pathways associated with endochondral and intramembranous bone development, caused perinatal lethality, and slowed chondrocyte and osteoblast differentiation in vitro. Transcriptomic analysis revealed that Hdac3 regulates vastly different pathways in mesenchymal cells expressing the Prxx1-Cre driver than those expressing the Col2-CreERT driver. Notably, Fgf21 was elevated in Hdac3-CKO
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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.