The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
NFATc1 in mice represses osteoprotegerin during osteoclastogenesis and dissociates systemic osteopenia from inflammation in cherubism
Open accessAbstract
Osteoporosis results from an imbalance in skeletal remodeling that favors bone resorption over bone formation. Bone matrix is degraded by osteoclasts, which differentiate from myeloid precursors in response to the cytokine RANKL. To gain insight into the transcriptional regulation of bone resorption during growth and disease, we generated a conditional knockout of the transcription factor nuclear factor of activated T cells c1 (Nfatc1). Deletion of Nfatc1 in young mice resulted in osteopetrosis and inhibition of osteoclastogenesis in vivo and in vitro. Transcriptional profiling revealed NFATc1 as a master regulator of the osteoclast transcriptome, promoting the expression of numerous genes needed for bone resorption. In addition, NFATc1 directly repressed osteoclast progenitor expression of osteoprotegerin, a decoy receptor for RANKL previously thought to be an osteoblast-derived inhibitor of bone resorption. "Cherubism mice", which carry a gain-of-function mutation in SH3-domain binding protein 2 (Sh3bp2), develop osteoporosis and widespread inflammation dependent on the proinflammatory cytokine, TNF-alpha. Interestingly, deletion of Nfatc1 protected cherubism mice from systemic bone loss but did not inhibit inflammation. Taken together, our study demonstrates that NFATc1 is required for remodeling of the growing and adult skeleton and suggests that NFATc1 may be an effective therapeutic target for osteoporosis associated with inflammatory states.
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Transcriptional regulation by calcium, calcineurin, and NFAT
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Autoamplification of NFATc1 expression determines its essential role in bone homeostasis
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TRANCE/RANKL knockout mice are protected from bone erosion in a serum transfer model of arthritis.
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Osteoclasts are essential for TNF-α-mediated joint destruction.
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Glucocorticoids suppress bone formation via the osteoclast.
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Identification of the membrane-type matrix metalloproteinase MT1-MMP in osteoclasts
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Cited by
Inflammation, fracture and bone repair
Loi, F., Córdova, L. A., Pajarinen, J., Lin, T.-H., Yao, Z., & Goodman, S. B. (2016) · Bone · doi:10.1016/j.bone.2016.02.020 · Cited by 1,293
Osteoclast differentiation by RANKL and OPG signaling pathways
Udagawa, N., Koide, M., Nakamura, M., Nakamichi, Y., Yamashita, T., Uehara, S., Kobayashi, Y., Furuya, Y., Yasuda, H., Fukuda, C., et al. (2021) · Journal of Bone and Mineral Metabolism · doi:10.1007/s00774-020-01162-6 · Cited by 708
Osteoclast differentiation factor RANKL controls development of progestin-driven mammary cancer
Schramek, D., Leibbrandt, A., Sigl, V., Kenner, L., Pospisilik, J. A., Lee, H. J., Hanada, R., Joshi, P. A., Aliprantis, A., Glimcher, L., et al. (2010) · Nature · doi:10.1038/nature09387 · Cited by 592
Self-citationRegulation of NFATc1 in Osteoclast Differentiation
Kim, J. H., & Kim, N. (2014) · Journal of Bone Metabolism · doi:10.11005/jbm.2014.21.4.233 · Cited by 570
“[15] NFATc1-deficient embryonic stem cells cannot differentiate into osteoclasts in response to RANKL.”
BackgroundOsteoimmunology: The conceptual framework unifying the immune and skeletal systems
Okamoto, K., Nakashima, T., Shinohara, M., Negishi-Koga, T., Komatsu, N., Terashima, A., Sawa, S., Nitta, T., & Takayanagi, H. (2017) · Physiological Reviews · doi:10.1152/physrev.00036.2016 · Cited by 534
Metadata
- Authors
- Aliprantis, A. O., Ueki, Y., Sulyanto, R., Park, A., Sigrist, K. S., Sharma, S. M., Ostrowski, M. C., Olsen, B. R., & Glimcher, L. H.
- Venue
- Journal of Clinical Investigation
- Published
- 2008-11-03
- Volume
- 118
- Issue
- 11
- Pages
- 3775-3789
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2143813009
- Cited by
- 350
- References
- 12
- FWCI
- 6.70
- Type
- journal article
- Language
- en
- Open access
- green
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- Aliprantis, A. O., Ueki, Y., Sulyanto, R., Park, A., Sigrist, K. S., Sharma, S. M., Ostrowski, M. C., Olsen, B. R., & Glimcher, L. H. (2008). NFATc1 in mice represses osteoprotegerin during osteoclastogenesis and dissociates systemic osteopenia from inflammation in cherubism. Journal of Clinical Investigation. https://doi.org/10.1172/jci35711
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