ArticleScientific reports2020
Hdac3 deletion in myeloid progenitor cells enhances bone healing in females and limits osteoclast fusion via Pmepa1.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- Old Blood, Young Bones: Identification of Middle-Aged Myeloid Cells That Limit Cortical Bone Loss.Journal of cellular and molecular medicine · 2026Article
- Elucidating the mechanisms by which acetyl tributyl citrate affects fracture healing: a comprehensive network toxicology study.BMC pharmacology & toxicology · 2026Article
- Decoding Epigenetic Switches: How Histone Acetylation/Deacetylation Regulates Mononuclear/Macrophage Fate in Bone Disorders.International journal of biological sciences · 2026Review
- Hdac3 deficiency limits periosteal reaction associated with Western diet feeding in female mice.Journal of cellular and molecular medicine · 2024Article
- Article
- Pulling rank with RNA: RANKL promotes the association of PGC-1β/RNA complexes with NCoR/HDAC3 to activate gene expression in osteoclasts.Molecular cell · 2023Article
- Macrophages and Bone Remodeling.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023Review
- Prostate transmembrane androgen inducible protein 1Frontiers in oncology · 2023Review
- Identification of a novel, MSC-induced macrophage subtype via single-cell sequencing: implications for intervertebral disc degeneration therapy.Frontiers in cell and developmental biology · 2023Article
- Article
- Histone deacetylase 3 (HDAC3) as an important epigenetic regulator of kidney diseases.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Two distinct resident macrophage populations coexist in the ovary.Frontiers in immunology · 2022Article
- Myeloid Lineage Ablation ofInternational journal of molecular sciences · 2021Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Previous studies examining the role of the histone deacetylase Hdac3 within myeloid cells demonstrated that Hdac3 promotes M2 activation and tissue healing in inflammatory conditions. Since myeloid lineage cells are required for proper bone formation and regeneration, in this study we examined the functions of Hdac3 during bone healing. Conditional deletion of Hdac3 within myeloid progenitors accelerates healing of cortical bone defects. Moreover, reduced osteoclast numbers within the defect site are correlated with Hdac3 suppression. Ex vivo osteoclastogenesis assays further demonstrate that Hdac3 deficiency limits osteoclastogenesis, the number of nuclei per cell and bone resorption, suggesting a defect in cell fusion. High throughput RNA sequencing identified the transmembrane protein Pmepa1 as a differentially expressed gene within osteoclast progenitor cells. Knockdown of Pmepa1 partially restores defects in osteoclastogenesis induced by Hdac3 deficiency. These results show that Hdac3 is required for optimal bone healing and osteoclast fusion, potentially via its regulation of Pmepa1 expression.
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