Hyperosmotic stimulus down-regulates 1α, 25-dihydroxyvitamin D 3-induced osteoclastogenesis by suppressing the RANKL expression in a co-culture system

Yu Shun Tian, Hyun Joo Jeong, Sang Do Lee, Seok Heui Kong, Seung Ho Ohk, Yun Jung Yoo, Jeong Taeg Seo, Dong Min Shin, Byung Wha Sohn, Syng Ill Lee

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1 Citation (Scopus)

Abstract

The hyperosmotic stimulus is regarded as a mechanical factor for bone remodeling. However, whether the hyperosmotic stimulus affects 1α, 25-dihydroxyvitamin D3 (1α,25(OH)2D 3)-induced osteoclastogenesis is not clear. In the present study, the effect of the hyperosmotic stimulus on 1α,25(OH)2D 3-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 1α,25(OH)2D3-induced tartrate-resistant acid phosphatase-positive multinucleated cells and 1α,25(OH)2D3-induced bone-resorbing pit area in a co-culture system. In osteoblastic cells, receptor activator of nuclear factor κB ligand (RANKL) and Runx2 expressions were down-regulated in response to 1α,25(OH)2D3. Knockdown of Runx2 inhibited 1α,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 1α,25(OH) 2D3-induced osteoclastogenesis, suppressing Runx2 and RANKL expression due to the TonEBP overexpression in osteoblastic cells.

Original languageEnglish
Pages (from-to)169-176
Number of pages8
JournalKorean Journal of Physiology and Pharmacology
Volume14
Issue number3
DOIs
Publication statusPublished - 2010 Jun

All Science Journal Classification (ASJC) codes

  • Physiology
  • Pharmacology

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