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The role of Mac‐1 (CD11b/CD18) in osteoclast differentiation induced by receptor activator of nuclear factor‐κB ligand
Author(s) -
Hayashi Hidetaka,
Nakahama Ken-ichi,
Sato Takahiro,
Tuchiya Takehiko,
Asakawa Yasuyuki,
Maemura Toshimitu,
Tanaka Masanobu,
Morita Mineto,
Morita Ikuo
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.08.023
Subject(s) - rankl , osteoclast , integrin alpha m , chemistry , cd11a , activator (genetics) , bone marrow , receptor , microbiology and biotechnology , antibody , cancer research , endocrinology , immunology , biology , cd18 , biochemistry
Multinuclear osteoclasts are derived from CD11b‐positive mononuclear cells in bone marrow and in circulation. FACS sorting experiments showed impaired osteoclastogenesis in RAW264.7 cells with low CD11b expression. Neutralizing antibodies and siRNA against CD11b inhibited osteoclastogenesis induced by RANKL. Although primary cultured mouse bone marrow macrophages expressed CD11a and CD11b, osteoclastogenesis induced by M‐CSF and RANKL was inhibited in the presence of anti‐CD11b or anti‐CD18 but not anti‐CD11a antibodies. Furthermore, anti‐CD11b antibodies inhibited NFATc1 expression induced by M‐CSF and RANKL in BMMs. These findings suggest, at least partly, an important role of CD11b in osteoclastogenesis.