Development of treatment and pathogenesis of implantation failure with a focus on the uterine cavity humoral factor

CD 9是一种24-kD的膜蛋白，其定位于内体和外泌体以及细胞膜上。缺乏cd 9的小鼠卵子无法与精子融合。本研究旨在探讨CD 9在子宫内膜中的作用。在仅CD 9表达于透明质膜（CD 9-/-TG）的转基因小鼠中，产后子宫内膜未被上皮覆盖，可见广泛粘连。在测量宫腔液的体液因子后，与野生型小鼠相比，CD 9-/-TG中的VEGF减少，因此认为CD 9的缺失可能干扰VEGF的产生。在CD 9基因敲除小鼠的子宫腔内注射VEGF后，子宫内膜上皮化。CD 9促进子宫内膜上皮细胞分泌VEGF，这些结果首次证明CD 9介导的VEGF分泌在子宫上皮再形成中起作用。

CD9 is a 24-kD membrane protein, which is localized on endosomes and exosomes as well as cell membranes. Cd9-deficient mouse eggs are unable to fuse with sperm. In this study, we intended that we focused on CD9 of the uterine cavity, and to clarify the role of CD9 in the endometrium. In transgenic mice that were rescued only CD9 expression in the zona pellucida (CD9-/-TG), endometrium of postpartum were not covered with the epithelium, were found extensive adhesions. After measurement of the humoral factors of the uterus cavity fluid, VEGF was decreased in CD9-/-TG compared with wild-type mice, so it was thought that loss of CD9 might interfere with VEGF production. When VEGF was injected in the uterine cavity of CD9 knockout mice, the endometrium was re-epithelialization. CD9 contributed to secretion of VEGF from endometrial epithelial cells, and these results provided the first evidence that CD9-mediated VEGF secretion plays a role in re-epithelialization of the uterus.