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High extracellular Ca2+ alone stimulates osteoclast formation but inhibits in the presence of other osteoclastogenic factors

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dc.contributor.authorKim, Gwan-Shik-
dc.contributor.authorShin, Myung-Mi-
dc.contributor.authorKim, Yong Hee-
dc.contributor.authorKim, Si Nae-
dc.contributor.authorBaek, Jeong-Hwa-
dc.date.accessioned2010-07-12T06:53:00Z-
dc.date.available2010-07-12T06:53:00Z-
dc.date.issued2003-06-
dc.identifier.citationExperimental and Molecular Medicine 2003;35:167-174en
dc.identifier.issn1226-3613-
dc.identifier.urihttps://hdl.handle.net/10371/68608-
dc.description.abstractHigh ambient Ca(2+) at bone resorption sites have been implicated to play an important role in the regulation of bone remodeling. The present study was performed to clarify the mode of high extracellular Ca(2+) (Ca(2+)(e))-induced modulation of osteoclastogenesis and the expression of receptor activator of nuclear factor-kappaB ligand (RANKL) and osteoprotegerin (OPG), thereby to define its role in osteoclast formation. Mouse bone marrow cells were cocultured with osteoblastic cells in the absence or presence of osteoclastogenic factors such as 1,25-dihydroxyvitaminD(3) (1,25-(OH)(2)vitD(3)) and macrophage colony-stimulating factor/soluble RANKL. Ca(2+) concentration in media (1.8 mM) was adjusted to 3, 5, 7 or 10 mM. Osteoclast formation was confirmed by the appearance of tartrate-resistant acid phosphatase (TRAP)-positive multinuclear cells and the expression of osteoclast phenotypic markers (calcitonin receptor, vitronectin receptor, cathepsin K, matrix metalloproteinase-9, carbonic anhydrase 2). High Ca(2+)(e) alone significantly stimulated osteoclast formation in a dose-dependent manner. However, in the presence of highly osteoclastogenic factors, high Ca(2+)(e) significantly inhibited osteoclastogenesis. High Ca(2+)(e) alone continuously up-regulated RANKL expression while only transiently increased OPG expression. However, in the presence of 1,25-(OH)(2)vitD(3), high Ca(2+)(e) did not change the 1,25-(OH)(2)vitD(3)-induced RANKL expression while increased OPG expression. Taken together, these findings suggest that high Ca(2+)(e) alone increase osteoclastogenesis but inhibit in the presence of other osteoclastogenic factors. In addition, high Ca(2+)(e)-induced osteoclastogenesis may be mediated by osteoblasts via up-regulation of RANKL expression. Meanwhile up-regulated OPG might participate in the inhibitory effect of high Ca(2+)(e) on 1,25-(OH)(2)vitD(3)-induced osteoclastogenesis.en
dc.language.isoenen
dc.publisherKorean Society of Medical Biochemistryen
dc.subjecthigh extracellular calciumen
dc.subjectosteoblasten
dc.subjectosteoclasten
dc.subjectosteoprotegerinen
dc.subjectRANKLen
dc.titleHigh extracellular Ca2+ alone stimulates osteoclast formation but inhibits in the presence of other osteoclastogenic factorsen
dc.typeArticleen
dc.contributor.AlternativeAuthor김관식-
dc.contributor.AlternativeAuthor신명미-
dc.contributor.AlternativeAuthor김영희-
dc.contributor.AlternativeAuthor김시내-
dc.contributor.AlternativeAuthor백정화-
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College of Dentistry/School of Dentistry (치과대학/치의학대학원)Dept. of Dentistry (치의학과)Journal Papers (저널논문_치의학과)
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