Compressive force stimulates the gene expression of IL-17s and their receptors in MC3T3-E1 cells.
Connect Tissue Res
; 51(5): 359-69, 2010 Oct.
Article
en En
| MEDLINE
| ID: mdl-20497006
During orthodontic tooth movement, cytokines released from periodontal ligament fibroblasts and alveolar bone osteoblasts can alter the process of bone remodeling. Recently, interleukin-17 (IL-17) was found to stimulate osteoclastic resorption through osteoblasts by inducing receptor activator of nuclear factor κB ligand (RANKL) expression. However, the relationship between mechanical stress and IL-17 production by osteoblasts is not clear. Therefore, we examined the effect of compressive force on the expressions of IL-17A, IL-17B, IL-17C, IL-17D, IL-17E, IL-17F, and their receptors (IL-17RA, IL-17RB, IL-17RC, IL-17RD, and IL-17RE) using MC3T3-E1 cells as osteoblast-like cells. We also examined the effect of IL-17A on the expression of IL-17Rs, RANKL, macrophage colony-stimulating factor (M-CSF), and osteoprotegerin (OPG). The cells were cultured with or without continuous compressive force (1.0 and 2.0 g/cm(2)) for up to 24 hr. The cells were also cultured with or without IL-17A (0.1, 1.0, or 10 ng/ml) for up to 72 hr. The mRNA expressions of IL-17s and their receptors were estimated by real-time polymerase chain reaction. The expression levels of IL-17s and their receptors increased depending on the compressive force. The addition of IL-17A increased the expression of IL-17RA, IL-17RB, IL-17RC, IL-17RE, RANKL, and M-CSF, whereas it decreased OPG expression. These results indicate that compressive force induces the expression of IL-17s and their receptors in osteoblast-like cells and that IL-17s and their receptors produced in response to compressive force may affect osteoclastogenesis through the expression of RANKL, M-CSF, and OPG.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Osteoblastos
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Estrés Mecánico
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Regulación de la Expresión Génica
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Fuerza Compresiva
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Interleucina-17
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Receptores de Interleucina-17
Límite:
Animals
Idioma:
En
Revista:
Connect Tissue Res
Año:
2010
Tipo del documento:
Article
País de afiliación:
China