ArticleAnnals of the New York Academy of Sciences2011
HDAC inhibitor trichostatin A suppresses osteoclastogenesis by upregulating the expression of C/EBP-β and MKP-1.
Article in Annals of the New York Academy of Sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Glucose metabolism in osteoporosis: A potential therapeutic target (Review).International journal of molecular medicine · 2026Review
- Lactylation's role in bone health and disease: mechanistic insights and therapeutic potential.PeerJ · 2025Review
- Histone Deacetylase 6 Inhibitor CKD-WID Suppressed Monosodium Urate-Induced Osteoclast Formation by Blocking Calcineurin-NFAT Pathway in RAW 264.7 Cells.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Attenuation of Rheumatoid Inflammation by Sodium Butyrate Through Reciprocal Targeting of HDAC2 in Osteoclasts and HDAC8 in T Cells.Frontiers in immunology · 2018Article
- Epigenetics and Bone Remodeling.Current osteoporosis reports · 2017Review
- Mitogen-activated protein kinase phosphatase 1 (MKP-1) in macrophage biology and cardiovascular disease. A redox-regulated master controller of monocyte function and macrophage phenotype.Free radical biology & medicine · 2017Review
- Histone Deacetylases in Bone Development and Skeletal Disorders.Physiological reviews · 2015Review
- Deletion of histone deacetylase 7 in osteoclasts decreases bone mass in mice by interactions with MITF.PloS one · 2015Article
- HDAC7 inhibits osteoclastogenesis by reversing RANKL-triggered β-catenin switch.Molecular endocrinology (Baltimore, Md.) · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Histone deacetylases (HDACs) remove the acetyl groups from the lysine residues of histone tails, leading to the formation of a condensed and transcriptionally silenced chromatin. HDAC inhibitors (HDACi) block this action and can result in hyperacetylation of histones, leading to a less compact and more transcriptionally active chromatin and thereby, gene expression. Previously, we have shown that HDACi inhibit osteoclast differentiation. However, which genes are transcriptionally activated following hyperacetylation of histones, and lead to the suppression of osteoclastogenesis, has yet to be elucidated. In this study, we show that an HDACi, trichostatin A (TSA), inhibits the receptor activator of the nuclear factor-κB (NF-κB) ligand (RANKL)-stimulated TNF-α production, NF-κB activation, and bone resorbing pit formation, and downregulates c-Fos and NFATc1 in RAW 264.7 cells. Interestingly, expression of antiosteoclastogenic factors CCAAT enhancer binding protein (C/EBP)-β and mitogen-activated protein kinase phosphatase (MKP)-1 was significantly upregulated in TSA-treated, RANKL-stimulated RAW 264.7 cells. These findings suggest that TSA upregulates the expression of C/EBP-β and MKP-1, which may downregulate pro-osteoclastogenic factors and signaling molecules, ultimately suppressing osteoclastogenesis.
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