南方医科大学学报2016，Vol.36Issue(9)：1209-1214,6.DOI:10.3969/j.issn.1673-4254.2016.09.08
p38 MAPK信号通路介导晚期氧化蛋白产物诱导的肾小管上皮细胞间充质转分化
P38 MAPK signaling pathway mediates advanced oxidation protein product-induced epithelial-to-mesenchymal transition in tubular cells
摘要
Abstract
Objective To investigate whether the p38 mitogen-activated protein kinase (MAPK) signaling pathway mediates advanced oxidation protein products (AOPPs)-induced epithelial-to-mesenchymal transition (EMT) in tubular cells. Methods Human proximal tubular cells (HK-2 cells) exposed to AOPP-bovine serum albumin (BSA) were examined for expressions of p38 MAPK and phosphorylated p38 MAPK using Western blotting. Western blotting and quantitative RT-PCR were used to examine the protein and mRNA expressions of EMT markers E-cadherin and vimentin and endoplasmic reticulum stress marker glucose-regulated protein (GRP) 78 in cells treated with SB203580 (an inhibitor of the p38 MAPK signaling pathway) prior to AOPP exposure. The cells treated with AOPPs following pretreatment with salubrinal (an inhibitor of endoplasmic reticulum stress) were also examined for expressions of p38 MAPK and phosphorylated p38 MAPK. Results AOPP treatment induced the phosphorylation of p38 MAPK in HK-2 cells. AOPP-induced decrease in E-cadherin expression and overexpression of vimentin and GRP78 were partly inhibited by pretreatment of the cells with SB203580. Salubrina partly suppressed AOPP-induced phosphorylation of p38 MAPK in the cells. Conclusion p38 MAPK signaling pathway, which is regulated by endoplasmic reticulum stress, might mediate AOPP-induced EMT in HK-2 cells.关键词
p38 MAPK/间充质转分化/晚期氧化蛋白产物/内质网应激/HK-2细胞Key words
p38 MAPK/epithelial-to-mesenchymal transition/advanced oxidation protein products/endoplasmic reticulum stress/HK-2 cells引用本文复制引用
黄丽丽,姜婷婷,汤珣,章俊,祝小林,邓伟谦,段娜,梁秀洁,王悦,郭婷婷,束双双,向晓红..p38 MAPK信号通路介导晚期氧化蛋白产物诱导的肾小管上皮细胞间充质转分化[J].南方医科大学学报,2016,36(9):1209-1214,6.基金项目
国家自然科学基金（81202842）；广州市科技计划项目（11C22120703）；广东省科技计划项目（2013B021800149）；广东省自然科学基金（S2011010004053，10151051501000030，S2011040003566）；中山市科技计划项目（2014A1FC085） Supported by National Natural Science Foundation of China (81202842) （81202842）
