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正常胎盘形态构建是胎盘功能及胎儿发育的关键,绒毛表面内层为细胞滋养细胞(CT),外层为合体滋养细胞(ST),CT分化融合形成ST,二者形成绒毛干,母体子宫动静脉开口于绒毛干间隙,构成母体胎儿胎盘循环。人内源性逆转录缺陷病毒(HERV)家族成员HERV-W编码的包膜蛋白syncyt-in可介导胎盘CT的生长分化。PE的病生特征是局部缺血缺氧,乏氧使syncytin表达下调。PE患者胎盘的syncytin蛋白表达下降,定位由正常的基底部ST细胞质膜转移到顶部ST微绒毛膜,syncytin mRNA转录水平也显著降低,使CT分化融合障碍、ST形成减少,胎盘形成不良,影响胎母血液循环、出现病理妊娠;但其syncytin受体ASCT2 mRNA水平无明显变化,syncytin与ASCT2 mRNA之间亦无线性相关性。syncytin是人类胎盘形态构成的必需要素,其表达障碍可干扰胎盘发育引发PE等病理妊娠,但syncytin与受体ASCT2的相互作用对PE发生的影响尚需深入研究。
Normal placenta morphogenesis is the key to placental function and fetal development. The inner layer of villus surface is cytotrophoblast (CT) and the outer layer is syncytiotrophoblast (ST). CT differentiation and fusion form ST, Vein openings in the hair dry gap, the formation of maternal fetal placental circulation. Syncyt-in, encoded by HERV-W, a member of the human endogenous reverse transcription deficient virus (HERV), mediates the growth and differentiation of placental CT. PE is characterized by ischemic disease hypoxia, hypoxia so that the expression of syncytin down. The expression of syncytin in placenta of PE patients decreased from the normal basal ST cell plasma membrane to the top of ST microvilli, and the transcription level of syncytin mRNA was also significantly decreased. The CT differentiation and fusion disorder, the reduction of ST formation, the placenta formation, However, there was no significant change in the level of ASCT2 mRNA in syncytin receptor and no linear correlation between syncytin and ASCT2 mRNA. Syncytin is an essential element in the formation of human placenta. The expression of syncytin may interfere with the development of placenta and lead to pathological pregnancy such as PE. However, the interaction between syncytin and ASCT2 still needs to be further studied.