Tetraspanin CD9 regulates osteoclastogenesis via regulation of p44/42 MAPK activity
- Department of Cell and Developmental Biology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul (Korea, Republic of)
- Department of Biochemistry, School of Dentistry, Kyungpook National University, Daegu (Korea, Republic of)
Tetraspanin CD9 has been shown to regulate cell-cell fusion in sperm-egg fusion and myotube formation. However, the role of CD9 in osteoclast, another multinucleated cell type, is not still clear. Therefore, we investigated the role of CD9 in osteoclast differentiation. CD9 was expressed in osteoclast lineage cells and its expression level increased during the progression of RANKL-induced osteoclastogenesis. KMC8, a neutralizing antibody specific to CD9, significantly suppressed RANKL-induced multinucleated osteoclast formation and the mRNA expression of osteoclast differentiation marker genes. To define CD9-regulated osteoclastogenic signaling pathway, MAPK pathways were examined. KMC8 induced long-term phosphorylation of p44/42 MAPK, but not of p38 MAPK. Constitutive activation of p44/42 MAPK by overexpressing constitutive-active mutant of MEK1 almost completely blocked osteoclast differentiation. Taken together, these results suggest that CD9 expressed on osteoclast lineage cells might positively regulate osteoclastogenesis via the regulation of p44/42 MAPK activity.
- OSTI ID:
- 20854415
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 347, Issue 1; Other Information: DOI: 10.1016/j.bbrc.2006.06.061; PII: S0006-291X(06)01364-7; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
Similar Records
Global epigenomic analysis indicates protocadherin-7 activates osteoclastogenesis by promoting cell–cell fusion
Ameloblastin and enamelin prevent osteoclast formation by suppressing RANKL expression via MAPK signaling pathway