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Compressive force induces the expression of bone remodeling-related proteins via interleukin-11 production in MC3T3-E1 cells

Abstract:
In bone remodeling during orthodontic tooth movement, osteoblasts are closely related to bone matrix formation and osteoclast differentiation. Interleukin (IL)-11 is known to be a regulating factor of bone remodeling. Our previous study showed that compressive force (CF) induced IL-11 production in osteoblastic Saos-2 cells. Therefore, we examined the effect of CF on the expression of IL-11 receptor (IL-11r), IL-11, Runx2, bone morphogenetic protein (BMP)-2, receptor activator of NF-κB ligand (RANKL), macrophage colony-stimulating factor (M-CSF), and osteoprotegerin (OPG) using MC3T3-E1 cells as osteoblasts. To confirm the participation of autocrine mechanisms by CF-induced IL-11, we also examined the effect of CF on expression in the presence and absence of IL-11 antagonist. MC3T3-E1 cells were cultured with or without continuous CF (1.0 or 2.0 g/ cm 2) in the presence or absence of IL-11 antagonist for up to 24 h. The expression of the IL-11r, IL-11, Runx2, BMP-2, RANKL, M-CSF, and OPG genes was estimated by determining mRNA levels by real-time PCR; protein expression was examined by ELISA or Western blotting. CF increased the expression of IL-11r and IL- 11; the maximum level of these expressions was achieved with CF at 2.0 g/cm 2. CF also increased the expression of Runx2 and BMP-2; the maximum level of these expressions was achieved in CF at 1.0 g/cm 2. IL-11 antagonist blocked the stimulatory effects of CF at 1.0 or 2.0 g/cm 2 on the expression of Runx2, BMP-2, RANKL, and M- CSF but not on the expression of IL-11r, IL-11, and OPG. These results suggest that CF at 1.0 g/cm 2 increases the expression of proteins related to bone formation, such as Runx2 and BMP-2, via the autocrine mechanism of CF-induced IL-11 in osteoblasts, whereas CF at 2.0 g/cm 2 increases the expression of RANKL and M-CSF that promotes osteoclast formation via CF-induced IL-11. These results also suggest that the balance of bone remodeling changes according to the strength of CF. © 2012The Hard Tissue Biology Network Association Printed in Japan, All rights reserved.

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Publisher copy:
10.2485/jhtb.21.65

Authors



Journal:
Journal of Hard Tissue Biology More from this journal
Volume:
21
Issue:
1
Pages:
65-74
Publication date:
2012-01-01
DOI:
EISSN:
1880-828X
ISSN:
1341-7649


Language:
English
Keywords:
Pubs id:
pubs:321516
UUID:
uuid:6282f70f-c3ba-4727-b926-dc2f74ed4710
Local pid:
pubs:321516
Source identifiers:
321516
Deposit date:
2013-11-17

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