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KMID : 0811720130170050427
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Korean Journal of Physiology & Pharmacology
2013 Volume.17 No. 5 p.427 ~ p.433
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Activation of G Proteins by Aluminum Fluoride Enhances RANKL- Mediated Osteoclastogenesis
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Park Bo-ryung
Yang Yu-Mi
Choi Byung-Jai
Kim Min-Seuk
Shin Dong-Min
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Abstract
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Receptor activator of NF-κB ligand (RANKL)-induced osteoclastogenesis is accompanied by intra-cellular Ca2＋ mobilization in a form of oscillations, which plays essential roles by activating sequen-tially Ca2＋/calmodulin-dependent protein kinase, calcineurin and NFATc1, necessary in the osteoclast differentiation. However, it is not known whether Ca2＋ mobilization which is evoked in RANKL-in-dependent way induces to differentiate into osteoclasts. In present study, we investigated Ca2＋ mobilization induced by aluminum fluoride (AlF4?), a G-protein activator, with or without RANKL and the effects of AlF4- on the osteoclastogenesis in primary cultured mouse bone marrow-derived macrophages (BMMs). We show here that AlF4? induces intracellular Ca2＋ concentration ([Ca2＋]i) oscillations, which is dependent on extracellular Ca2＋ influx. Notably, co-stimulation of AlF4? with RANKL resulted in enhanced NFATc1 expression and formation of tartrate-resistant acid phosphatase (TRAP) positive multinucleated cells. Additionally, we confirmed that mitogen-activated protein kinase (MAPK) is also activated by AlF4-. Taken together, these results demonstrate that G-protein would be a novel modulator responsible for [Ca2＋]i oscillations and MAPK activation which lead to enhancement of RANKL-mediated osteoclastogenesis.
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KEYWORD
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AlF4-, Ca2＋ signaling, G protein, MAPK activation, Osteoclastogenesis
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