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. 2015 Dec 3;6(12):e2009. doi: 10.1038/cddis.2015.350

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Copyright © 2015 Macmillan Publishers Limited

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Mechanisms of gingival fibroblasts in cell apoptosis resistance. LPS-induced ROS accumulation in acute inflammation. DNA damage appeared as time went on. Finally, apoptosis was detectable in chronic periodontitis. Short after stimulation, LPS increased phosphorylated ERK1/2, phosphorylated p38, phosphorylated JNK, p53, BCL-2, and Survivin in a dose-dependent manner. Simultaneously, phosphorylated AKT decreases in a dose-dependent manner. As a result, the anti-apoptotic effects and pro-apoptotic effects were balanced. The expression of p53 and p21, the ratio of LC3 ІI/LC3 I were increased by LPS, indicating senescence and autophagy were involved, respectively