文章基本信息

标题：p38 Mitogen-Activated Protein Kinase is Involved in Endoplasmic Reticulum Stress-Induced Cell Death and Autophagy in Human Gingival Fibroblasts
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作者：Do-Sung Kim ; Jung-Hoon Kim ; Geum-Hwa Lee 等
期刊名称：Biological and Pharmaceutical Bulletin
印刷版ISSN：0918-6158
电子版ISSN：1347-5215
出版年度：2010
卷号：33
期号：4
页码：545-549
DOI：10.1248/bpb.33.545
出版社：The Pharmaceutical Society of Japan
摘要：Inflammation or hypoxia in gingival tissue can induce endoplasmic reticulum (ER) stress, which is related with autophagy. The autophagy is a catabolic process involving the degradation of a cell's own components. Although autophagy resulting in the total destruction of the cell is one of cell death types, no conclusive evidence exists for such a process. In order to examine the association of ER stress and autophagy in gingival system, ER stress agents brefeldin A, thapsigargin, and tunicamycin were exposed to human gingival cells. The ER stress agents induced cell death and the expression of ER stress proteins, glucose-regulated protein of 78 kDa (GRP78) and CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP). ER stress also increased the formation of autophagic vesicles with the expression of beclin and LC-3 (microtubule-associated protein1 light chain 3) II, two autophagic markers. ER stress induced the phosphorylation of p38MAPK (mitogen-activated protein kinase), and the p38MPAK inhibitor, SB203580, inhibited the resulting cell death and autophagy. In summary, ER stress induces cell death and autophagy through p38MAPK in human gingival cells.
关键词：endoplasmic reticulum stress;autophagy;cell death;p38 mitogen-activated kinase;glucose regulated protein 78;CCAAT/enhancer-binding protein homologous protein