Hyperosmotic Stimulus Down-regulates 1alpha, 25-dihydroxyvitamin D3-induced Osteoclastogenesis by Suppressing the RANKL Expression in a Co-culture System.
10.4196/kjpp.2010.14.3.169
- Author:
Yu Shun TIAN
1
;
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
Author Information
1. Department of Oral Biology, Yonsei University, Seoul 120-752, Korea. lsi@yuhs.ac
- Publication Type:Original Article
- Keywords:
Hyperosmotic stimulus;
TonEBP;
Osteoblast;
RANKL;
Runx2
- MeSH:
Bone Remodeling;
Coculture Techniques;
Down-Regulation;
Osteoblasts;
RANK Ligand;
Sucrose
- From:The Korean Journal of Physiology and Pharmacology
2010;14(3):169-176
- CountryRepublic of Korea
- Language:English
-
Abstract:
The hyperosmotic stimulus is regarded as a mechanical factor for bone remodeling. However, whether the hyperosmotic stimulus affects 1alpha, 25-dihydroxyvitamin D3 (1alpha,25(OH)2D3)-induced osteoclastogenesis is not clear. In the present study, the effect of the hyperosmotic stimulus on 1alpha,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 1alpha,25(OH)2D3-induced tartrate-resistant acid phosphatase-positive multinucleated cells and 1alpha,25(OH)2D3-induced bone-resorbing pit area in a co-culture system. In osteoblastic cells, receptor activator of nuclear factor kappaB ligand (RANKL) and Runx2 expressions were down-regulated in response to 1alpha,25(OH)2D3. Knockdown of Runx2 inhibited 1alpha,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 1alpha,25(OH)2D3-induced osteoclastogenesis, suppressing Runx2 and RANKL expression due to the TonEBP overexpression in osteoblastic cells.
