TY - JOUR
T1 - Hyperosmotic stimulus down-regulates 1α, 25-dihydroxyvitamin D 3-induced osteoclastogenesis by suppressing the RANKL expression in a co-culture system
AU - Tian, Yu Shun
AU - Jeong, Hyun Joo
AU - Lee, Sang Do
AU - Kong, Seok Heui
AU - Ohk, Seung Ho
AU - Yoo, Yun Jung
AU - Seo, Jeong Taeg
AU - Shin, Dong Min
AU - Sohn, Byung Wha
AU - Lee, Syng Ill
N1 - Funding Information:
I would like to thank Ministry of Education Malaysia for supporting the research with the grant FRGS/2/2013/TK01/UKM/02/1.
PY - 2010/6
Y1 - 2010/6
N2 - 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.
AB - 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.
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U2 - 10.4196/kjpp.2010.14.3.169
DO - 10.4196/kjpp.2010.14.3.169
M3 - Article
C2 - 20631890
AN - SCOPUS:77954894543
SN - 1226-4512
VL - 14
SP - 169
EP - 176
JO - Korean Journal of Physiology and Pharmacology
JF - Korean Journal of Physiology and Pharmacology
IS - 3
ER -