Death receptors, Fas and TRAIL receptors, are involved in human osteoclast apoptosis
| Autor: | Pascal Lambert-Comeau, Sophie Roux, Céline Saint-Pierre, Mariette Lépine, Bassem Sawan, Jean-Luc Parent |
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| Rok vydání: | 2005 |
| Předmět: |
musculoskeletal diseases
Biophysics Osteoclasts Apoptosis Biochemistry Monocytes Receptors Tumor Necrosis Factor TNF-Related Apoptosis-Inducing Ligand Multinucleate Osteoclast medicine Humans fas Receptor Calcitonin receptor Receptor Molecular Biology Cells Cultured Membrane Glycoproteins biology Tumor Necrosis Factor-alpha Cell Differentiation Cell Biology Cell biology medicine.anatomical_structure RANKL Cord blood biology.protein Antibody Apoptosis Regulatory Proteins |
| Zdroj: | Biochemical and biophysical research communications. 333(1) |
| ISSN: | 0006-291X |
| Popis: | Survival and apoptosis are crucial aspects of the osteoclast life cycle. Although osteoclast survival has been extensively studied, little is known about the mechanisms involved in human osteoclast apoptosis. In the present study, cord blood monocytes (CBMs) were used as the source of human osteoclast precursors. When cultured in the presence of M-CSF and RANKL, CBMs formed multinucleated cells that expressed RANK and calcitonin receptor, and were able to resorb bone. These cells expressed TRAIL receptors (R1-R4). Surprisingly, although TRAIL-receptor expression was not detectable in osteoclasts from normal bone, osteoclasts from myeloma specimens did express TRAIL receptors to a variable extent. Significantly, we have shown for the first time that this pathway is indeed functional in human osteoclasts, and that apoptosis occurred and was significantly greater in the presence of TRAIL. In addition, we have shown that a Fas-activating antibody is also able to induce osteoclast apoptosis, as did TGFbeta, whereas the survival factor M-CSF decreased apoptosis. Overall, these findings suggest that death receptors, TRAIL receptors and Fas, could be involved in osteoclast apoptosis in humans. |
| Databáze: | OpenAIRE |
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