4-Hydroxynonenal induces an increase in expression of Receptor for Activating C Kinase 1 (RACK1) in Chinese hamster V79-4 lung cells
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- 作者：Dan Lia ; b ; lidan@mail.cmu.edu.cn" class="auth_mail ; Elizabeth M. Ellisb
- 关键词：HNE ; 4-hydroxy-trans-2-nonenal ; PMSF ; (phenylmethansulfonyl fluoride) ; ROS ; reactive oxygen species ; D ; dimension ; TOF ; time of flight ; MTT ; 3-(4 ; 5-dimethylthiazoyl-2-yl)-2 ; 5-diphenyltetrazolium bromide ; MALDI ; matrix-assisted laser desorption/ionization ; G protein ; guanine nucleotide binding protein
- 刊名：Chemico-Biological Interactions
- 出版年：25 April, 2014
- 年：2014
- 卷：213
- 期：Complete
- 页码：13-20
- 全文大小：1678 K
文摘
4-Hydroxy-trans-2-nonenal (HNE) is a cytotoxic 伪,尾-unsaturated aldehyde implicated in the pathology of several diseases that have an oxidative stress mechanism, including atherosclerosis, diabetes, alcohol-induced liver disease, and neurodegenerative disorders. As the most toxic aldehydic product of lipid peroxidation, HNE is known to exert a range of biological effects in a concentration-dependent manner. In this study, the effect of HNE on the levels of proteins in V79-4 Chinese hamster lung cells was investigated using two-dimensional electrophoresis and mass spectrometry. The results revealed that the expression of 23 proteins was increased by at least 2-fold and the expression of 19 proteins was decreased by at least 2-fold after exposure to 10 渭M HNE for 24 h. Decreased proteins included the metabolic enzyme phosphoglycerate kinase 1 (PGK1), levels of which were decreased by 47%. Levels of the apoptotic indicator Lamin C were decreased by 33%. In contrast, levels of the scaffolding protein Receptor for Activating C Kinase 1 (RACK1) were increased by 2-fold after treatment with 10 渭M HNE for 24 h, and this was confirmed using quantitative PCR of reverse-transcribed mRNA and Western blots. The role of RACK1 in mediating the induction of apoptosis in response to 10 渭M HNE was confirmed using RACK1-specific siRNA. The results from this study provide new information on the mechanism of adaptive stress response to HNE and also identify potential new biomarkers of exposure to HNE.