Hyperosmotic Stimulus Down-regulates 1alpha, 25-dihydroxyvitamin D(3)-induced Osteoclastogenesis by Suppressing the RANKL Expression in a Co-culture System.
Korean J Physiol Pharmacol
; 14(3): 169-76, 2010 Jun.
Article
en En
| MEDLINE
| ID: mdl-20631890
ABSTRACT
The hyperosmotic stimulus is regarded as a mechanical factor for bone remodeling. However, whether the hyperosmotic stimulus affects 1alpha, 25-dihydroxyvitamin D(3) (1alpha,25(OH)(2)D(3))-induced osteoclastogenesis is not clear. In the present study, the effect of the hyperosmotic stimulus on 1alpha,25(OH)(2)D(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 1alpha,25(OH)(2)D(3)-induced tartrate-resistant acid phosphatase-positive multinucleated cells and 1alpha,25(OH)(2)D(3)-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)(2)D(3). Knockdown of Runx2 inhibited 1alpha,25(OH)(2)D(3)-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)(2)D(3)-induced osteoclastogenesis, suppressing Runx2 and RANKL expression due to the TonEBP overexpression in osteoblastic cells.
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01-internacional
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MEDLINE
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En
Revista:
Korean J Physiol Pharmacol
Año:
2010
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Article