Journal
KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
Volume 17, Issue 5, Pages 427-433Publisher
KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
DOI: 10.4196/kjpp.2013.17.5.427
Keywords
AlF4-; Ca2+ signaling; G protein; MAPK activation; Osteoclastogenesis
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Funding
- National Research Foundation of Korea (NRF)
- Korea government (MEST) [2012R1A2A1A01003487, 2007-0056092, 2012R1A1A1038381]
- National Research Foundation of Korea [2012R1A1A1038381, 2012R1A2A1A01003487] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Receptor activator of NF-kappa B ligand (RANKL)-induced osteoclastogenesis is accompanied by intracellular Ca2+ mobilization in a form of oscillations, which plays essential roles by activating sequentially 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-independent 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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