ArticleThe Journal of pathology2018
C/ebpα controls osteoclast terminal differentiation, activation, function, and postnatal bone homeostasis through direct regulation of Nfatc1.
Article in The Journal of pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Transcriptome Analysis of Differentially Expressed Genes and Molecular Pathways Involved During Osteoclast Differentiation.Molecular biotechnology · 2026Article
- Targeting CEBPA/ALOX15B attenuates postmenopausal osteoporosis by inhibiting ferroptosis through the AMPK/mTOR signaling pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Cell signaling and transcriptional regulation of osteoclast lineage commitment, differentiation, bone resorption and diseases.Cell discovery · 2026Review
- Integrative single-cell RNA-seq and ATAC-seq identifies transcriptional and epigenetic blueprint guiding osteoclastogenic trajectory.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025Article
- Cell signaling and transcriptional regulation of osteoblast lineage commitment, differentiation, bone formation, and homeostasis.Cell discovery · 2024Review
- Osteoporosis: interferon-gamma-mediated bone remodeling in osteoimmunology.Frontiers in immunology · 2024Review
- Role and Regulation of Transcription Factors in Osteoclastogenesis.International journal of molecular sciences · 2023Review
- Effects of urolithin A on osteoclast differentiation induced by receptor activator of nuclear factor-κB ligand via bone morphogenic protein 2.Bioengineered · 2022Article
- GPR125 positively regulates osteoclastogenesis potentially through AKT-NF-κB and MAPK signaling pathways.International journal of biological sciences · 2022Article
- Knockout and Double Knockout of Cathepsin K and Mmp9 reveals a novel function of Cathepsin K as a regulator of osteoclast gene expression and bone homeostasis.International journal of biological sciences · 2022Article
- Selumetinib - a potential small molecule inhibitor for osteoarthritis treatment.Frontiers in pharmacology · 2022Article
- Role of Biomolecules in Osteoclasts and Their Therapeutic Potential for Osteoporosis.Biomolecules · 2021Review
- LY3023414 inhibits both osteogenesis and osteoclastogenesis through the PI3K/Akt/GSK3 signalling pathway.Bone & joint research · 2021Article
- Gone Caving: Roles of the Transcriptional Regulators YAP and TAZ in Skeletal Development.Current osteoporosis reports · 2020Review
- At the Crossroads of the Adipocyte and Osteoclast Differentiation Programs: Future Therapeutic Perspectives.International journal of molecular sciences · 2020Review
- F2r negatively regulates osteoclastogenesis through inhibiting the Akt and NFκB signaling pathways.International journal of biological sciences · 2020Article
- Regulation of Osteoclast Differentiation and Skeletal Maintenance by Histone Deacetylases.Molecules (Basel, Switzerland) · 2019Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Osteoclast lineage commitment and differentiation have been studied extensively, although the mechanism by which transcription factor(s) control osteoclast terminal differentiation, activation, and function remains unclear. CCAAT/enhancer-binding protein α (C/ebpα) has been reported to be a key regulator of osteoclast cell lineage commitment, yet C/ebpα's roles in osteoclast terminal differentiation, activation and function, and bone homeostasis, under physiological or pathological conditions, have not been studied because newborn C/ebpα-null mice die within several hours after birth. Furthermore, the function of C/ebpα in osteoclast terminal differentiation, activation, and function is largely unknown. Herein, we generated and analyzed an osteoclast-specific C/ebpα conditional knockout (CKO) mouse model via Ctsk-Cre mice and found that C/ebpα-deficient mice exhibited a severe osteopetrosis phenotype due to impaired osteoclast terminal differentiation, activation, and function, including mildly reduced osteoclast number, impaired osteoclast polarization, actin formation, and bone resorption, which demonstrated the novel function of C/ebpα in cell function and terminal differentiation. Interestingly, C/ebpα deficiency did not affect bone formation or monocyte/macrophage development. Our results further demonstrated that C/ebpα deficiency suppressed the expression of osteoclast functional genes, e.g. encoding cathepsin K (Ctsk), Atp6i (Tcirg1), and osteoclast regulator genes, e.g. encoding c-fos (Fos), and nuclear factor of activated T-cells 1 (Nfatc1), while having no effect on Pu.1 (Spi1) expression. Promoter activity mapping and ChIP assay defined the critical cis-regulatory element (CCRE) in the promoter region of Nfatc1, and also showed that the CCREs were directly associated with C/ebpα, which enhanced the promoter's activity. The deficiency of C/ebpα in osteoclasts completely blocked ovariectomy-induced bone loss, indicating that C/ebpα is a promising new target for the treatment of osteolytic diseases. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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