摘要
目的:探讨米非司酮对人胚胎细胞JAR与人子宫内膜细胞RL95-2之间黏附的影响及其调控的分子机制。方法:采用黏附实验分别观察RU486以及岩藻糖基转移酶IV(FUT4)对JAR细胞与RL95-2细胞之间黏附的影响。采用RT-PCR以及Western blotting检测米非司酮对RL95-2细胞以及流产妇女子宫内膜中FUT4表达的调控。结果:①米非司酮抑制JAR细胞与RL95-2单层细胞之间的黏附;②米非司酮抑制RL95-2细胞以及流产妇女子宫内膜中FUT4基因和蛋白的表达;③FUT4质粒转染RL95-2细胞后,调节JAR细胞与RL95-2单层细胞之间的黏附。结论:米非司酮通过调节FUT4的表达抑制胚胎体外黏附。
Objective: To investigate the effect of mifepristone on the adhesion of JAR cells to RL95-2 cells monolayer and its regulation mechanism. Methods: The adhesion of JAR cells to RL95-2 cells monolayer which was treated with mifepristone or fucosyltransferase IV (FUT4) plasmid was detected by cell counting. The regulation of mifepristone via FUT4 in RL95-2 cells and in human endometfial tissues was examined by RT-PCR and Western blotting. Results: 1) Mifepristone inhibited the adhesion of JAR cells to RL95-2 cells monolayer. 2) Mifepristone inhibited the expression of FUT4 in RL95-2 cells and in human endometrial tissues by RT-PCR and Western blotting. 3) The adhesion of JAR cells to RL95-2 cell monolayer was inhibited by FUT4-siRNA. Inversely, the percent of adhesion was promoted by FUT4 over-expression plasmid. Conclusion: Mifepristone inhibits the adhesion of embryos in vitro by decreasing the expression of FUT4.
出处
《生殖与避孕》
CAS
CSCD
2014年第1期1-5,26,共6页
Reproduction and Contraception