Xu Yan-qiong, Li Ai-ping, Chen Rui, Zhou Jian-wei
Department of Molecular Cell Biology & Toxicology, School of Public Health, Nanjing Medical University, Nanjing 210029, China.
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2006 Apr;24(4):205-8.
To investigate the role and possible mechanism of JWA in N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) induced human bronchial epithelial (HBE) cell apoptosis.
The cell growth inhibition rate was detected by MTT, the cell apoptosis was measured by Hoechst staining, the expression of JWA protein was detected by Western blot, and the potential binding protein of JWA proximal promoter was detected by Southwestern assay.
MNNG treatment of HBE cells for 24 hours induced apoptosis with significant dose-effect relationship and in this course the expression of JWA protein was elevated. The 2.0 microg/ml MNNG treated cells for 24 hours activated nuclear transcription factor expression that specifically bound to JWA proximal promoter.
That MNNG treatment activates nuclear transcription factor binding to JWA proximal promoter may be involved in intracellular apoptosis associated signal pathway.
探讨JWA在N-甲基-N'-硝基-N-亚硝基胍(MNNG)诱导的人支气管上皮(HBE)细胞凋亡中的作用及可能机制。
采用MTT法检测细胞生长抑制率,Hoechst染色法检测细胞凋亡,Western blot法检测JWA蛋白表达,Southwestern法检测JWA近端启动子潜在结合蛋白。
MNNG处理HBE细胞24小时可诱导细胞凋亡,呈明显的剂量-效应关系,此过程中JWA蛋白表达升高。2.0μg/ml MNNG处理细胞24小时可激活与JWA近端启动子特异性结合的核转录因子表达。
MNNG处理激活与JWA近端启动子结合的核转录因子可能参与细胞内凋亡相关信号通路。