ArticleBone2009
NFATc1 mediates HDAC-dependent transcriptional repression of osteocalcin expression during osteoblast differentiation.
Article in Bone, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
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The trial behind it
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Who cites it
55 citing papers in PubMed, 86 citations in OpenAlex.
- CaMKIV negatively regulates osteoblast differentiation by modulating c-Fos and NFATc1 signaling: an in vitro and in vivo mechanistic study.BMB reports · 2026Article
- TGF-β/BMP signaling in skeletal biology: molecular mechanisms, regulatory networks, and therapeutic implications in development, regeneration, and disease.Bone research · 2026Review
- Bioactive deproteinized bovine bone mineral based on self-assembled albumin nanoparticles promoted bone regeneration via activation of Wnt/β-catenin pathway.Materials today. Bio · 2025Article
- Review
- Unlocking the Epigenetic Symphony: Histone Acetylation Orchestration in Bone Remodeling and Diseases.Stem cell reviews and reports · 2025Review
- Enhanced Osteogenic Potential ofACS biomaterials science & engineering · 2023Article
- The Osteogenesis Imperfecta Type V Mutant BRIL/IFITM5 Promotes Transcriptional Activation of MEF2, NFATc, and NR4A in Osteoblasts.International journal of molecular sciences · 2022Article
- Genetics and Epigenetics of Bone Remodeling and Metabolic Bone Diseases.International journal of molecular sciences · 2022Review
- Estrogen receptor alpha and NFATc1 bind to a bone mineral density-associated SNP to repress WNT5B in osteoblasts.American journal of human genetics · 2022Article
- The role of CaCell proliferation · 2021Review
- Epigenetic reprogramming enhances the therapeutic efficacy of osteoblast-derived extracellular vesicles to promote human bone marrow stem cell osteogenic differentiation.Journal of extracellular vesicles · 2021Article
- The Roles of Epigenetics Regulation in Bone Metabolism and Osteoporosis.Frontiers in cell and developmental biology · 2020Review
- Harnessing the HDAC-histone deacetylase enzymes, inhibitors and how these can be utilised in tissue engineering.International journal of oral science · 2019Review
- Hepatic Osteodystrophy-Molecular Mechanisms Proposed to Favor Its Development.International journal of molecular sciences · 2019Review
- Deletion of Orai1 leads to bone loss aggravated with aging and impairs function of osteoblast lineage cells.Bone reports · 2018Article
- Effect of β‑ecdysterone on glucocorticoid‑induced apoptosis and autophagy in osteoblasts.Molecular medicine reports · 2018Article
- An update on the role of epigenetics in systemic vasculitis.Current opinion in rheumatology · 2018Review
- Histone deacetylases and their roles in mineralized tissue regeneration.Bone reports · 2017Review
- Bone regeneration with osteogenic matrix cell sheet and tricalcium phosphate: An experimental study in sheep.World journal of orthopedics · 2017Article
- Concise Review: Stem Cells in Osteoimmunology.Stem cells (Dayton, Ohio) · 2017Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
We previously reported that the in vivo and in vitro suppression of Nuclear Factor of Activated T Cells (NFAT) signaling increases osteoblast differentiation and bone formation. To investigate the mechanism by which NFATc1 regulates osteoblast differentiation, we established an osteoblast cell line that overexpresses a constitutively active NFATc1 (ca-NFATc1). The activation of NFATc1 significantly inhibits osteoblast differentiation and function, demonstrated by inhibition of alkaline phosphatase activity and mineralization as well as a decrease in gene expression of early and late markers of osteoblast differentiation such as osterix and osteocalcin, respectively. By focusing on the specific role of NFATc1 during late differentiation, we discovered that the inhibition of osteocalcin gene expression by NFATc1 was associated with a repression of the osteocalcin promoter activity, and a decrease in TCF/LEF transactivation. Also, overexpression of NFATc1 completely blocked the decrease in total histone deacetylase (HDAC) activity during osteoblast differentiation and prevented the hyperacetylation of histones H3 and H4. Mechanistically, we show by Chromatin Immunoprecipitation (ChIP) assay that the overexpression of NFATc1 sustains the binding of HDAC3 on the proximal region of the osteocalcin promoter, resulting in complete hypoacetylation of histones H3 and H4 when compared to GFP-expressing osteoblasts. In contrast, the inhibition of NFATc1 nuclear translocation either by cyclosporin or by using primary mouse osteoblasts with deleted calcineurin b1 prevents HDAC3 from associating with the proximal regulatory site of the osteocalcin promoter. These preliminary results suggest that NFATc1 acts as a transcriptional co-repressor of osteocalcin promoter, possibly in an HDAC-dependent manner.
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What OpenQuestion holds
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.