Bone stromal cells in pagetic bone and Paget's sarcoma express RANKL and support human osteoclast formation
Autor: | N A Athanasou, Y S Lau, S G Sun, I Itonaga, Afsie Sabokbar |
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Rok vydání: | 2006 |
Předmět: |
Male
musculoskeletal diseases Pathology medicine.medical_specialty Stromal cell medicine.medical_treatment Gene Expression Osteoclasts Receptors Cytoplasmic and Nuclear Bone Neoplasms Cell Communication Receptors Tumor Necrosis Factor Pathology and Forensic Medicine Bone remodeling Biological Factors Osteoprotegerin Osteoclast otorhinolaryngologic diseases medicine Humans RNA Messenger RNA Neoplasm Cells Cultured Aged Glycoproteins Aged 80 and over Osteosarcoma Membrane Glycoproteins Receptor Activator of Nuclear Factor-kappa B biology Reverse Transcriptase Polymerase Chain Reaction business.industry RANK Ligand Osteitis Deformans medicine.disease Coculture Techniques medicine.anatomical_structure Cytokine RANKL biology.protein Sarcoma Stromal Cells Carrier Proteins business |
Zdroj: | The Journal of Pathology. 209:114-120 |
ISSN: | 1096-9896 0022-3417 |
DOI: | 10.1002/path.1953 |
Popis: | Paget's disease is a focal disorder of bone remodelling, in which there is an increase in osteoclast formation. A rare complication of Paget's disease is the development of a sarcoma, most commonly an osteosarcoma. Osteoclast formation occurs in the presence of macrophage-colony stimulating factor and receptor activator for nuclear factor-κB ligand (RANKL), and it has been shown that bone stromal cells in Paget's disease can influence osteoclast formation by modulating the expression of RANKL and its decoy receptor, osteoprotegerin (OPG). In this study we show that pagetic bone stromal cells express RANKL and that these cells promote osteoclast formation by a RANKL-dependent mechanism. Osteoclast formation in co-cultures of monocytes and either pagetic bone stromal cells or Paget's sarcoma stromal cells was not only induced by a contact-dependent mechanism but also occurred via the release of a soluble factor. In contrast to bone stromal cells isolated from normal controls, stromal cells isolated from morphologically normal bone in one patient with Paget's disease also stimulated osteoclast formation in this way; this osteoclastogenesis was inhibited by OPG. Our results indicate that Paget's bone stromal cells support osteoclast formation by a RANKL-dependent process which involves not only cell–cell contact but also secretion of soluble RANKL. Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. |
Databáze: | OpenAIRE |
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