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Compressive mechanical stress may activate IKK-NF-κB through proinflammatory cytokines in MC3T3-E1 cells
Ying Lu1, Qinghua Zheng, Wanlu Lu
1State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China, 532335421@qq.com.
Objective:
To determine whether IKK-NF-κB is activated either directly by compressive mechanical stress or by proinflammatory cytokines produced by MC3T3-E1 cells under compressive stress loading.
Results:
MC3T3-E1 cells subjected to cyclic uniaxial compressive stress showed increased expression of proinflammatory cytokines and activation of the IKK-NF-κB signaling pathway with nuclear translocation of p65. Following treatment with antibodies to neutralize the action of the proinflammatory cytokines, IL-1β and IL-6, the activation of IKK-NF-κB signaling was notably inhibited in MC3T3-E1 cells subjected to force loading.
Conclusion:
IKK-NF-κB signaling in MC3T3-E1 cells may be activated by proinflammatory cytokines that are produced as a consequence of mechanical stress loading and not by direct compressive mechanical stress.
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