p53基因在内质网应激诱导的晶状体上皮细胞凋亡中的作用  

The Effect of p53 on Endoplasmic Reticulum Stress-induced Apoptosis of Lens Epithelial Cells

作　　者：赵学英[1] 高顺玉[2] 李树德[3] 张远平[1] 冯维杨[3] 

机构地区：[1]昆明医学院第二附属医院眼科,云南昆明650101 [2]云南大学生命科学学院,云南昆明650091 [3]昆明医学院生化教研室,云南昆明650031

出　　处：《昆明医学院学报》2009年第1期36-38,53,共4页Journal of Kunming Medical College

摘　　要：目的探讨在内质网应激诱导的晶状体上皮细胞凋亡中,p53基因的作用.方法衣霉素用于诱导晶状体上皮细胞株LEC内质网应激.细胞凋亡用Hoechst染色法.基因表达测定采用RT-PCR.结果衣霉素处理导致CHOP基因表达升高,LEC细胞凋亡率和caspase-3活性增加.同时,衣霉素诱导细胞p53表达升高.通过转染的方式过表达CHOP基因可加强衣霉素诱导的LEC细胞凋亡以及p53表达升高.但是仅仅过表达CHOP基因并不能诱导LEC细胞凋亡以及p53表达升高.结论p53基因很可能在内质网应激所介导的细胞凋亡起重要作用,但p53基因不是CHOP的直接靶基因.Objective To investigate the effect of p53 on endoplasmic reticulum stress-induced apoptosis of lens epithelial cells （LEC）.Methods Endoplasmic reticulum stress was induced by tunicamycin in LEC. The apoptosis of LEC was determined by Hoechst staining.The expression of genes was detected by RT-PCR. Results Tunicamycin treatment resulted in increased expression of CHOP,the rate of apoptosis as well as the activity of caspase-3 in LEC.Meanwhile, tunicamycin treatment also up-regulated the expression of p53. Overexpression of CHOP by transfection enhanced tunicamycin-medaited apoptosis and the expression of p53 in LEC.However,Overexpression of CHOP alone did not induce apoptosis and the expression of p53 in LEC. Conclusion p53 plays a critical role in endoplasmic reticulum stress-induced apoptosis of LEC.However,p53 is not the direct targeted gene of CHOP.

关 键 词：CHOP 内质网应激 晶状体上皮细胞 细胞凋亡 p53 

分 类 号：R776[医药卫生—眼科]