TDRKH基因对NIH3T3细胞凋亡的影响  

Role of TDRKHgene on NIH3T3 cell apoptosis

作　　者：陈洪艳[1] 徐明强[1] 王嘉玮[1] 刘畅[1] 付瑶[1] 高妍[1] 姜昊[1] 戴立胜[1] 张嘉保[1] 

机构地区：[1]吉林大学动物科学学院,吉林长春130062

出　　处：《中国兽医学报》2017年第1期154-158,共5页Chinese Journal of Veterinary Science

基　　金：现代农业产业技术体系专项资金资助项目(CARS-38)

摘　　要：使用NIH3T3细胞进行试验,利用RNAi方法抑制TDRKH的mRNA的表达水平。通过流式细胞术、RTqPCR等方法分别检测细胞凋亡情况及凋亡相关基因Bcl-2、Bax等的表达变化。结果显示:敲减TDRKH表达并不会明显导致NIH3T3细胞的凋亡,凋亡相关基因Bax、P53mRNA表达量无显著性变化,但Bcl-2、Survivin mRNA表达量显著下降,Bcl-2/Bax值显著降低。结果表明:TDRKH虽然不能直接诱导细胞凋亡,但可通过其他潜在基因调控通路影响细胞功能。TDRDS（tudor domain containing proteins） protein family can identify the methylate ar- ginine- modified mark and plays a unique role in the process of male germ cell development. As a member of the TDRDS, TDRKH is involved in the primary piRNA maturation and the occurrence of male germ cells through its interaction with Miwi/Miwi2. TDRKH plays a key role in the mei- osis of male animals. The male TDRKH gene knock-out mice are infertile, but the mechanism is unclear. NIH3T3 cell was used for experiment and the RNAi was used to inhibit the mRNA ex- pression of TDRKH. Flow cytometry and RT-qPCR were used to respectively test the cell apop- tosis and expression change of relevant genes such as Bcl-2 and Bax. The results showed that knockdown TDRKH could not increase the apoptosis rate of NIH3T3, and the expression of P53, Bax mRNA was no significant change, but the expression of Bcl-2, survivin mRNA was down-reg- ulated in TDRKH knockdown groups, and the expression of Bcl-2/Bax mRNA was down-regula- ted simultaneously. It shows that TDRKH dose not directly induce apoptosis , but may affect cell function by other potential gene regulatory pathways.

关 键 词：NIH3T3 TDRKH RNA干扰 细胞凋亡 

分 类 号：S852.3[农业科学—基础兽医学]