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KMID : 0811720100140030169
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Korean Journal of Physiology & Pharmacology
2010 Volume.14 No. 3 p.169 ~ p.176
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Hyperosmotic Stimulus Down-regulates 1?, 25-dihydroxyvitamin D3- induced Osteoclastogenesis by Suppressing the RANKL Expression in a Co-culture System
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Tian Yu-Shun
Jeong Hyun-Joo
Lee Sang-Do
Kong Seok-Heui
Ohk Seung-Ho
Yu Yoon-Jeong
Seo Jeong-Taeg
Shin Dong-Min
Sohn Byung-Wha
Lee Syng-Ill
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Abstract
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The hyperosmotic stimulus is regarded as a mechanical factor for bone remodeling. However, whether the hyperosmotic stimulus affects 1?, 25-dihydroxyvitamin D3 (1?,25(OH)2D3)-induced osteoclastogenesis is not clear. In the present study, the effect of the hyperosmotic stimulus on 1?,25(OH)2D3- induced osteoclastogenesis was investigated in an osteoblast-preosteoclast co-culture system. Serial doses of sucrose were applied as a mechanical force. These hyperosmotic stimuli significantly evoked a reduced number of 1?,25(OH)2D3-induced tartrate-resistant acid phosphatase-positive multinucleated cells and 1?,25(OH)2D3-induced bone-resorbing pit area in a co-culture system. In osteoblastic cells, receptor activator of nuclear factor ?B ligand (RANKL) and Runx2 expressions were down-regulated in response to 1?,25(OH)2D3. Knockdown of Runx2 inhibited 1?,25(OH)2D3-induced RANKL expression in osteoblastic cells. Finally, the hyperosmotic stimulus induced the overexpression of TonEBP in osteoblastic cells. These results suggest that hyperosmolarity leads to the down-regulation of 1?,25(OH)2D3- induced osteoclastogenesis, suppressing Runx2 and RANKL expression due to the TonEBP overexpression in osteoblastic cells.
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KEYWORD
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Hyperosmotic stimulus, TonEBP, Osteoblast, RANKL, Runx2
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