Mysteries in Ca2+ signaling during osteoclast differentiation
Mysteries in Ca2+ signaling during osteoclast differentiation
复制标题
破骨细胞分化过程中 Ca2 信号传导的奥秘
DOI：
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发表时间：
2009
期刊：
影响因子：
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通讯作者：
H. Takayanagi
中科院分区：
文献类型：
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作者：
Takako Negishi;H. Takayanagi
Nuclear factor of activated T cells c1 (NFATc1) activation by Ca signaling is an essential part of the signaling axis in osteoclast differentiation. Although the molecular signaling cascade downstream of receptor activator of nuclear factor-κB ligand (RANKL) has been extensively studied, the origin of the intracellular Ca increase and the dynamics required for efficient NFATc1 activation have been unclear. Using mice lacking inositol 1,4,5-triphosphate (IP3) receptor (IP3R) type 2 (IP3R2) and IP3R3, a study from last year by Kuroda and coauthors found that RANKL-induced Ca oscillation and osteoclast differentiation were impaired in vitro, but that there was no defect in osteoclastogenesis in vivo (1). To understand this discrepancy, the authors focused on the role of osteoblasts, which have the ability to induce osteoclastogenesis in IP3R2/3-deficient cells. Surprisingly, Ca oscillation was not detected in the coculture system, but NFATc1 induction and osteoclastogenesis were observed. Their findings suggest the existence of an as yet unidentified (possibly Ca oscillationindependent) regulatory mechanism for NFATc1 activation mediated by osteoblasts, and may open up new directions for research on Ca signaling during osteoclastogenesis.
影响因子：
8.7
作者：
F. Ross;S. Teitelbaum
通讯作者：
F. Ross;S. Teitelbaum
影响因子：
10.5
作者：
Yang, Shuying;Li, Yi-Ping
通讯作者：
Li, Yi-Ping