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Fibroblastic stromal cells express receptor activator of NF-kappa B ligand and support osteoclast differentiation.
J Bone Miner Res. 2000 Aug; 15(8):1459-66.JB

Abstract

Osteoclast formation in bone is supported by osteoblasts expressing receptor activator of NF-kappa B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) expression. Numerous osteotropic factors regulate expression levels of RANKL and the RANKL decoy receptor osteoprotegerin (OPG) in osteoblasts, thereby affecting osteoclast differentiation. However, not only in RANKL widely expressed in soft tissues, but osteoclasts have been noted in extraskeletal lesions. We found that cultured skin fibroblastic cells express RANKL, M-CSF, and OPG messenger (mRNA). Stimulation by 1 alpha,25 dihydroxyvitamin D3 [1,25(OH)2D3] plus dexamethasone (Dex) augmented RANKL and diminished OPG mRNA expression in fibroblastic cells and caused the formation of numerous osteoclasts in cocultures of skin fibroblastic cells with hemopoietic cells or monocytes. The osteoclasts thus formed expressed tartrate-resistant acid phosphatase (TRAP) and calcitonin (CT) receptors and formed resorption pits in cortical bone. Osteoclast formation also was stimulated (in the presence of Dex) by prostaglandin E2 (PGE2), interleukin-11 (IL-11), IL-1, tumor necrosis factor-alpha (TNF-alpha), and parathyroid hormone-related protein (PTHrP), factors which also stimulate osteoclast formation supported by osteoblasts. In addition, granulocyte-macrophage-CSF (GM-CSF), transforming growth factor-beta (TGF-beta), and OPG inhibited osteoclast formation in skin fibroblastic cell-hemopoietic cell cocultures; CT reduced only osteoclast nuclearity. Fibroblastic stromal cells from other tissues (lung, respiratory diaphragm, spleen, and tumor) also supported osteoclast formation. Thus, RANKL-positive fibroblastic cells in extraskeletal tissues can support osteoclastogenesis if osteolytic factors and osteoclast precursors are present. Such mesenchymally derived cells may play a role in pathological osteolysis and may be involved in osteoclast formation in extraskeletal tissues.

Authors+Show Affiliations

St. Vincent's Institute of Medical Research, Fitzroy, Victoria, Australia.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10934644

Citation

Quinn, J M., et al. "Fibroblastic Stromal Cells Express Receptor Activator of NF-kappa B Ligand and Support Osteoclast Differentiation." Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research, vol. 15, no. 8, 2000, pp. 1459-66.
Quinn JM, Horwood NJ, Elliott J, et al. Fibroblastic stromal cells express receptor activator of NF-kappa B ligand and support osteoclast differentiation. J Bone Miner Res. 2000;15(8):1459-66.
Quinn, J. M., Horwood, N. J., Elliott, J., Gillespie, M. T., & Martin, T. J. (2000). Fibroblastic stromal cells express receptor activator of NF-kappa B ligand and support osteoclast differentiation. Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research, 15(8), 1459-66.
Quinn JM, et al. Fibroblastic Stromal Cells Express Receptor Activator of NF-kappa B Ligand and Support Osteoclast Differentiation. J Bone Miner Res. 2000;15(8):1459-66. PubMed PMID: 10934644.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fibroblastic stromal cells express receptor activator of NF-kappa B ligand and support osteoclast differentiation. AU - Quinn,J M, AU - Horwood,N J, AU - Elliott,J, AU - Gillespie,M T, AU - Martin,T J, PY - 2000/8/10/pubmed PY - 2001/2/28/medline PY - 2000/8/10/entrez SP - 1459 EP - 66 JF - Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research JO - J Bone Miner Res VL - 15 IS - 8 N2 - Osteoclast formation in bone is supported by osteoblasts expressing receptor activator of NF-kappa B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) expression. Numerous osteotropic factors regulate expression levels of RANKL and the RANKL decoy receptor osteoprotegerin (OPG) in osteoblasts, thereby affecting osteoclast differentiation. However, not only in RANKL widely expressed in soft tissues, but osteoclasts have been noted in extraskeletal lesions. We found that cultured skin fibroblastic cells express RANKL, M-CSF, and OPG messenger (mRNA). Stimulation by 1 alpha,25 dihydroxyvitamin D3 [1,25(OH)2D3] plus dexamethasone (Dex) augmented RANKL and diminished OPG mRNA expression in fibroblastic cells and caused the formation of numerous osteoclasts in cocultures of skin fibroblastic cells with hemopoietic cells or monocytes. The osteoclasts thus formed expressed tartrate-resistant acid phosphatase (TRAP) and calcitonin (CT) receptors and formed resorption pits in cortical bone. Osteoclast formation also was stimulated (in the presence of Dex) by prostaglandin E2 (PGE2), interleukin-11 (IL-11), IL-1, tumor necrosis factor-alpha (TNF-alpha), and parathyroid hormone-related protein (PTHrP), factors which also stimulate osteoclast formation supported by osteoblasts. In addition, granulocyte-macrophage-CSF (GM-CSF), transforming growth factor-beta (TGF-beta), and OPG inhibited osteoclast formation in skin fibroblastic cell-hemopoietic cell cocultures; CT reduced only osteoclast nuclearity. Fibroblastic stromal cells from other tissues (lung, respiratory diaphragm, spleen, and tumor) also supported osteoclast formation. Thus, RANKL-positive fibroblastic cells in extraskeletal tissues can support osteoclastogenesis if osteolytic factors and osteoclast precursors are present. Such mesenchymally derived cells may play a role in pathological osteolysis and may be involved in osteoclast formation in extraskeletal tissues. SN - 0884-0431 UR - https://www.unboundmedicine.com/medline/citation/10934644/Fibroblastic_stromal_cells_express_receptor_activator_of_NF_kappa_B_ligand_and_support_osteoclast_differentiation_ L2 - https://doi.org/10.1359/jbmr.2000.15.8.1459 DB - PRIME DP - Unbound Medicine ER -