Abstract
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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Acknowledgments
This work was supported by National Natural Science Foundation of China (Nos. 11472183 and 81300876) and accomplished in the State Key Laboratory of Oral Diseases, West China College of Stomatology, Sichuan University, Chengdu, China.
Supporting Information
Supplementary Table 1—Gene-specific primers for qPCR.
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Lu, Y., Zheng, Q., Lu, W. et al. Compressive mechanical stress may activate IKK-NF-κB through proinflammatory cytokines in MC3T3-E1 cells. Biotechnol Lett 37, 1729–1735 (2015). https://doi.org/10.1007/s10529-015-1849-6
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DOI: https://doi.org/10.1007/s10529-015-1849-6