期刊
MOLECULES AND CELLS
卷 36, 期 3, 页码 252-257出版社
KOREAN SOC MOLECULAR & CELLULAR BIOLOGY
DOI: 10.1007/s10059-013-0159-x
关键词
bone; gene expression; osteoclast differentiation; RANKL; SLAT
资金
- National Research Foundation of Korea (NRF) [2011-0030132]
- Korea government [Ministry of Science, Ict & Future Planning (MSIP)]
- Korean Health Technology R&D Project, Ministry of Health Welfare [HI11C0674]
RANKL induces the formation of osteoclasts, which are responsible for bone resorption. Herein, we investigated the role of SWAP-70-like adapter of T cells (SLAT) in RANKL-induced osteoclastogenesis. Expression levels of SLAT were reduced during RANKL-induced osteoclastogenesis. Overexpression of SLAT in BMMs inhibited TRAP-positive multinuclear osteoclast formation and attenuated the expression of NFATc1, which is an important modulator in osteoclastogenesis. Furthermore, silencing of SLAT by RNA interference enhanced osteoclast formation as well as NFATc1 expression. In addition, SLAT was involved in RANKL-induced JNK activation in osteoclasts. Taken together, our data suggest that SLAT acts as a negative modulator of RANKL-induced osteoclastogenesis.
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