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

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.