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J Bone Miner Res. 2003 Mar;18(3):443-50.

TRAF5 functions in both RANKL- and TNFalpha-induced osteoclastogenesis.

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1
Department of Life Science, Tokyo Institute of Technology, Yokohama, Japan.

Abstract

Although TRAF6 is essential for both RANKL- and TNFalpha-induced osteoclastogenesis, it has remained unclear whether other members of the TRAF family are involved in osteoclastogenesis. We examined TRAF5 function in both RANKL- and TNFalpha-induced osteoclastogenesis by using osteoclast progenitor cells from TRAF5-deficient mice. The results demonstrated that RANKL or TNFalpha 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 NF-kappaB activation was apparently observed in osteoclast progenitor cells. In the parathyroid hormone (PTH)-induced hypercalcemia model, calcium concentration peaked at day 3 after administration. However, in TRAF5-deficient mice, this peak was delayed and found at day 5, showing less effective osteoclast differentiation. Thus, we have provided the first evidence showing that TRAF5 is involved in osteoclastogenesis.

PMID:
12619928
DOI:
10.1359/jbmr.2003.18.3.443
[Indexed for MEDLINE]
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