粘附分子CD44在母胎界面和妊娠相关疾病中的研究进展  

The research progress of adhesion molecules CD44 in maternal-fetal interface and pregnancy-related diseases

作　　者：鲜舒 杨潇[1] 王艳青[1] 程艳香[1] 

机构地区：[1]武汉大学人民医院妇产科,武汉430060

出　　处：《中国优生与遗传杂志》2017年第8期1-4,共4页Chinese Journal of Birth Health & Heredity

基　　金：国家自然科学基金(项目编号81302273);湖北省卫计委一般面上项目(项目编号WJ2015MB084);湖北省科技厅科技项目支撑计划(2015BCA313)

摘　　要：正常妊娠的发生赖于滋养细胞对子宫内膜的适度浸润。粘附分子CD44(cluster of differentiation 44)是一类普遍存在的多结构和多功能细胞表面分子,在母胎界面的表达具有时空特异性,能与透明质酸(Hyaluronan,HA)、基质金属蛋白酶(matrix metalloproteinases,MMPs)相互作用,激活PI3K/AKT、MAPK/ERK1/2信号通路,调控绒毛外滋养细胞对子宫内膜基质的侵袭和迁移。此外,母胎界面中转化生长因子-β1(transforming growth factor-β1,TGF-β1)的差异性表达也可能通过CD44调控滋养细胞侵袭性质;CD44-MMPs复合物也可反馈调节炎症介质的释放,形成有利于胚胎着床和发育的免疫耐受微环境。当CD44及其特异亚型如CD44v3/6表达异常时,可致使妊娠失败或妊娠相关疾病的发生。A successful pregnancy depends on the appropriate invasion of trophoblastic cells on the endometrium. The adhesion molecule CD44 is a ubiquitous multi-structural and multi-functional cell surface molecule involved. The expression of CD44 and its isoforms is dynamic spatiotemporal in the maternal-fetal interface,which can interact with HA and MMPs to activate PI3K/AKT and MAPK/ERK1/2 signaling pathways,resulting in regulation of trophoblast invasion and migration through the endometrial stroma. In addition,the differential expression of TGF-β1 in the maternal-fetal interface can regulate the invasiveness of trophoblast through CD44;CD44-MMPs complexes can also adjust the release of inflammatory mediators,which is conducive to the formation of embryo implantation and development as well as immune tolerance microenvironment. Abnormal expression of CD44 and its specific subtypes such as CD44v3/6,can lead to pregnancy failure or Pregnancy-related diseases.

关 键 词：CD44 CD44V 滋养细胞 母胎界面 

分 类 号：R714.2[医药卫生—妇产科学]