Osteoblasts/stromal cells stimulate osteoclast activation through expression of osteoclast differentiation factor/RANKL but not macrophage colony-stimulating factor: receptor activator of NF-kappa B ligand - PubMed (original) (raw)
doi: 10.1016/s8756-3282(99)00210-0.
N Takahashi, E Jimi, K Matsuzaki, T Tsurukai, K Itoh, N Nakagawa, H Yasuda, M Goto, E Tsuda, K Higashio, M T Gillespie, T J Martin, T Suda
Affiliations
- PMID: 10574571
- DOI: 10.1016/s8756-3282(99)00210-0
Osteoblasts/stromal cells stimulate osteoclast activation through expression of osteoclast differentiation factor/RANKL but not macrophage colony-stimulating factor: receptor activator of NF-kappa B ligand
N Udagawa et al. Bone. 1999 Nov.
Abstract
We previously reported that osteoblasts/stromal cells are essentially involved in the activation as well as differentiation of osteoclasts through a mechanism involving cell-to-cell contact between osteoblasts/stromal cells and osteoclast precursors/osteoclasts. Osteoclast differentiation factor (ODF, also called RANKL/OPGL/TRANCE) and macrophage colony-stimulating factor (M-CSF, also called CSF-1) are two essential factors produced by osteoblasts/stromal cells for osteoclastogenesis. In other words, osteoblasts/stromal cells were not necessary to generate osteoclasts from spleen cells in the presence of both ODF/RANKL and M-CSF. In the present study, we examined the precise roles of ODF/RANKL and M-CSF in the activation of osteoclasts induced by calvarial osteoblasts. Osteoclasts were formed in mouse bone marrow cultures on collagen gel-coated dishes in response to a soluble form of ODF/RANKL (sODF/sRANKL) and M-CSF, and recovered by collagenase digestion. When recovered osteoclasts were further cultured on plastic dishes, most of the osteoclasts spontaneously died within 24 h. Osteoclasts cultured for 24 h on dentine slices could not form resorption pits. Addition of sODF/sRANKL to the recovered osteoclasts markedly enhanced their survival and pit-forming activity. M-CSF similarly stimulated the survival of osteoclasts, but did not induce their pit-forming activity. When primary mouse osteoblasts were added to the recovered osteoclasts, resorption pits were formed on dentine slices. Bone-resorbing factors such as 1alpha,25-dihydroxyvitamin D3, parathyroid hormone, or prostaglandin E2 enhanced pit-forming activity of osteoclasts only in the presence of osteoblasts. M-CSF-deficient osteoblasts prepared from op/op mice similarly enhanced pit-forming activity of osteoclasts. The pit-forming activity of osteoclasts induced by sODF/sRANKL or osteoblasts was completely inhibited by simultaneous addition of osteoprotegerin/osteoclastogenesis inhibitory factor, a decoy receptor of ODF/RANKL. Primary osteoblasts constitutively expressed ODF/RANKL mRNA, and its level was upregulated by treatment with 1alpha,25-dihydroxyvitamin D3, parathyroid hormone, and prostaglandin E2. These results, obtained by using an assay system that unequivocally assesses osteoclast activation, suggest that ODF/RANKL but not M-CSF mediates osteoblast-induced pit-forming activity of osteoclasts, and that bone-resorbing factors stimulate osteoclast activation through upregulation of ODF/RANKL by osteoblasts/stromal cells.
Similar articles
- Importance of membrane- or matrix-associated forms of M-CSF and RANKL/ODF in osteoclastogenesis supported by SaOS-4/3 cells expressing recombinant PTH/PTHrP receptors.
Itoh K, Udagawa N, Matsuzaki K, Takami M, Amano H, Shinki T, Ueno Y, Takahashi N, Suda T. Itoh K, et al. J Bone Miner Res. 2000 Sep;15(9):1766-75. doi: 10.1359/jbmr.2000.15.9.1766. J Bone Miner Res. 2000. PMID: 10976996 - Roles of macrophage-colony stimulating factor and osteoclast differentiation factor in osteoclastogenesis.
Tsurukai T, Udagawa N, Matsuzaki K, Takahashi N, Suda T. Tsurukai T, et al. J Bone Miner Metab. 2000;18(4):177-84. doi: 10.1007/s007740070018. J Bone Miner Metab. 2000. PMID: 10874596 - The molecular basis of osteoclast differentiation and activation.
Suda T, Kobayashi K, Jimi E, Udagawa N, Takahashi N. Suda T, et al. Novartis Found Symp. 2001;232:235-47; discussion 247-50. doi: 10.1002/0470846658.ch16. Novartis Found Symp. 2001. PMID: 11277084 Review. - A new member of tumor necrosis factor ligand family, ODF/OPGL/TRANCE/RANKL, regulates osteoclast differentiation and function.
Takahashi N, Udagawa N, Suda T. Takahashi N, et al. Biochem Biophys Res Commun. 1999 Mar 24;256(3):449-55. doi: 10.1006/bbrc.1999.0252. Biochem Biophys Res Commun. 1999. PMID: 10080918 Review.
Cited by
- In vitro osteoclastogenesis in autoimmune diseases - Strengths and pitfalls of a tool for studying pathological bone resorption and other disease characteristics.
Skubica P, Husakova M, Dankova P. Skubica P, et al. Heliyon. 2023 Nov 3;9(11):e21925. doi: 10.1016/j.heliyon.2023.e21925. eCollection 2023 Nov. Heliyon. 2023. PMID: 38034780 Free PMC article. Review. - Osteoclasts at Bone Remodeling: Order from Order.
Takito J, Nonaka N. Takito J, et al. Results Probl Cell Differ. 2024;71:227-256. doi: 10.1007/978-3-031-37936-9_12. Results Probl Cell Differ. 2024. PMID: 37996681 Review. - Nuclear Factor-Kappa B Regulation of Osteoclastogenesis and Osteoblastogenesis.
Boyce BF, Li J, Yao Z, Xing L. Boyce BF, et al. Endocrinol Metab (Seoul). 2023 Oct;38(5):504-521. doi: 10.3803/EnM.2023.501. Epub 2023 Sep 26. Endocrinol Metab (Seoul). 2023. PMID: 37749800 Free PMC article. - Assembling the Puzzle Pieces. Insights for in Vitro Bone Remodeling.
Krasnova O, Neganova I. Krasnova O, et al. Stem Cell Rev Rep. 2023 Aug;19(6):1635-1658. doi: 10.1007/s12015-023-10558-6. Epub 2023 May 19. Stem Cell Rev Rep. 2023. PMID: 37204634 Review. - The Serotonergic System and Bone Metabolism During Pregnancy and Lactation and the Implications of SSRI Use on the Maternal-Offspring Dyad.
Fricke HP, Hernandez LL. Fricke HP, et al. J Mammary Gland Biol Neoplasia. 2023 Apr 22;28(1):7. doi: 10.1007/s10911-023-09535-z. J Mammary Gland Biol Neoplasia. 2023. PMID: 37086330 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Research Materials
Miscellaneous