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Tumor Necrosis Factor α‐Induced Osteoclastogenesis Requires Tumor Necrosis Factor Receptor‐Associated Factor 6
Author(s) -
Kaji Keisuke,
Katogi Rei,
Azuma Yoshiaki,
Naito Asuka,
Inoue JunIchiro,
Kudo Akira
Publication year - 2001
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1359/jbmr.2001.16.9.1593
Subject(s) - rankl , osteoclast , tumor necrosis factor alpha , rank ligand , progenitor cell , cancer research , activator (genetics) , medicine , endocrinology , receptor , biology , microbiology and biotechnology , stem cell
Although tumor necrosis factor receptor‐associated factor 6 (TRAF6) is required in receptor activator of NF‐κB‐receptor activator of NF‐κB ligand (RANK‐RANKL) signaling for osteoclastogenesis, it has remained unclear whether TRAF6 is crucial in tumor necrosis factor α (TNF‐α)‐induced osteoclastogenesis. We examined TRAF6 function in the TNF‐α‐induced osteoclastogenesis by using osteoclast progenitor cells from TRAF6‐deficient mice. The results indicated that TNF‐α did not effectively induce osteoclast differentiation from osteoclast progenitor cells derived from these mice into mature multinucleated osteoclasts, although c‐ jun N‐terminal kinase (JNK) and TNF‐α activation was observed in osteoclast progenitor cells. Thus, we have provided the first evidence showing that TRAF6 is involved in TNF‐α‐induced osteoclastogenesis.