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Effects of mechanical stress on cytokine production in mandible-derived osteoblasts

Oral Diseases (2011) 17, 712–719 Objective:  Mechanical stress is known to be an important factor in the regulation of bone remodeling, and mandibular bone is continuously exposed to mechanical stressors such as occlusal force. Therefore, in this study, we investigated the effects of mechanical stre...

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Published in:Oral diseases 2011-10, Vol.17 (7), p.712-719
Main Authors: Yamamoto, K, Yamamoto, T, Ichioka, H, Akamatsu, Y, Oseko, F, Mazda, O, Imanishi, J, Kanamura, N, Kita, M
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cited_by cdi_FETCH-LOGICAL-c5832-13831c29bf70771c455cc1027c85b6819ea0167a6d7ca8e0bd0480d590e1c3163
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container_start_page 712
container_title Oral diseases
container_volume 17
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Yamamoto, T
Ichioka, H
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description Oral Diseases (2011) 17, 712–719 Objective:  Mechanical stress is known to be an important factor in the regulation of bone remodeling, and mandibular bone is continuously exposed to mechanical stressors such as occlusal force. Therefore, in this study, we investigated the effects of mechanical stress approaching occlusal force, to which mandible‐derived osteoblasts (MDOB) are exposed, on cytokine expression and production using an original hydrostatic pressure apparatus. Materials and Methods:  The levels of cytokine in MDOB were examined by real‐time RT‐PCR, ELISA, and western blotting. In addition, mitogen‐activated protein kinase inhibitor for ERK1/2, JNK, and p‐38 pathways was used to identify the signal transduction pathway. Results:  Hydrostatic pressure increased the expression of IL‐6 and TNF‐α mRNA in a magnitude‐ and time‐dependent manner and also enhanced IL‐6 and TNF‐α protein production. Furthermore, hydrostatic pressure changed the RANKL/OPG ratio in favor of RANKL for both mRNA and protein levels. Specific inhibitor of p‐38 pathway but not that of the ERK1/2 and JNK pathways suppressed the up‐regulation of RANKL production induced by hydrostatic pressure loading. Conclusion:  These results suggest that MDOB play a role in cytokine production in response to mechanical stress and that occlusal force may support the maintenance of mandible bone homeostasis by activating bone remodeling through osteoclastogenesis.
doi_str_mv 10.1111/j.1601-0825.2011.01832.x
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Therefore, in this study, we investigated the effects of mechanical stress approaching occlusal force, to which mandible‐derived osteoblasts (MDOB) are exposed, on cytokine expression and production using an original hydrostatic pressure apparatus. Materials and Methods:  The levels of cytokine in MDOB were examined by real‐time RT‐PCR, ELISA, and western blotting. In addition, mitogen‐activated protein kinase inhibitor for ERK1/2, JNK, and p‐38 pathways was used to identify the signal transduction pathway. Results:  Hydrostatic pressure increased the expression of IL‐6 and TNF‐α mRNA in a magnitude‐ and time‐dependent manner and also enhanced IL‐6 and TNF‐α protein production. Furthermore, hydrostatic pressure changed the RANKL/OPG ratio in favor of RANKL for both mRNA and protein levels. Specific inhibitor of p‐38 pathway but not that of the ERK1/2 and JNK pathways suppressed the up‐regulation of RANKL production induced by hydrostatic pressure loading. 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Therefore, in this study, we investigated the effects of mechanical stress approaching occlusal force, to which mandible‐derived osteoblasts (MDOB) are exposed, on cytokine expression and production using an original hydrostatic pressure apparatus. Materials and Methods:  The levels of cytokine in MDOB were examined by real‐time RT‐PCR, ELISA, and western blotting. In addition, mitogen‐activated protein kinase inhibitor for ERK1/2, JNK, and p‐38 pathways was used to identify the signal transduction pathway. Results:  Hydrostatic pressure increased the expression of IL‐6 and TNF‐α mRNA in a magnitude‐ and time‐dependent manner and also enhanced IL‐6 and TNF‐α protein production. Furthermore, hydrostatic pressure changed the RANKL/OPG ratio in favor of RANKL for both mRNA and protein levels. Specific inhibitor of p‐38 pathway but not that of the ERK1/2 and JNK pathways suppressed the up‐regulation of RANKL production induced by hydrostatic pressure loading. 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Therefore, in this study, we investigated the effects of mechanical stress approaching occlusal force, to which mandible‐derived osteoblasts (MDOB) are exposed, on cytokine expression and production using an original hydrostatic pressure apparatus. Materials and Methods:  The levels of cytokine in MDOB were examined by real‐time RT‐PCR, ELISA, and western blotting. In addition, mitogen‐activated protein kinase inhibitor for ERK1/2, JNK, and p‐38 pathways was used to identify the signal transduction pathway. Results:  Hydrostatic pressure increased the expression of IL‐6 and TNF‐α mRNA in a magnitude‐ and time‐dependent manner and also enhanced IL‐6 and TNF‐α protein production. Furthermore, hydrostatic pressure changed the RANKL/OPG ratio in favor of RANKL for both mRNA and protein levels. Specific inhibitor of p‐38 pathway but not that of the ERK1/2 and JNK pathways suppressed the up‐regulation of RANKL production induced by hydrostatic pressure loading. 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subjects Alkaline Phosphatase - analysis
Animals
Biomechanical Phenomena
Bite Force
Blotting, Western
Bone Remodeling - physiology
Bone remodelling
Cells, Cultured
Cytokines
Cytokines - biosynthesis
Dentistry
Enzyme-Linked Immunosorbent Assay
Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors
Hydrostatic Pressure
inflammatory cytokine
Interleukin-6 - biosynthesis
Kinases
Male
Mandible - cytology
Mandible - metabolism
MAP Kinase Kinase 4 - antagonists & inhibitors
MAP Kinase Signaling System - drug effects
mechanical stress
Mice
Mice, Inbred C57BL
Mice, Inbred Strains
OPG
osteoblast
Osteoblasts - metabolism
Osteoprotegerin - biosynthesis
p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors
Proteins
RANK Ligand - biosynthesis
RANKL
Real-Time Polymerase Chain Reaction
Reverse Transcriptase Polymerase Chain Reaction
Signal transduction
Stress, Mechanical
Tumor Necrosis Factor-alpha - biosynthesis
title Effects of mechanical stress on cytokine production in mandible-derived osteoblasts
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