子痫前期是妊娠期特有疾病，严重威胁母儿健康。子宫螺旋动脉血管重铸不良引起胎盘缺血缺氧，是子痫前期发生的重要病理基础，以滋养细胞侵润障碍，内皮细胞凋亡减少为特点，但调控机制不明。本课题组前期研究发现子痫前期患者血清中转甲状腺素蛋白（transthyretin，TTR）明显降低。已有研究发现TTR可结合可溶性溶酶体相关膜蛋白-1（lysosome-associated membrane protein，LAMP-1），引起LAMP-1的聚集，减少其向溶酶体膜上转化。而LAMP-1是维持溶酶体膜稳定性的重要蛋白，可减少溶酶体诱导的细胞凋亡。我们最新研究也显示添加TTR可降低人脐静脉内皮细胞膜蛋白中LAMP-1的含量，因此本研究以TTR影响LAMP-1转化为研究基础，探讨TTR通过LAMP-1影响内皮细胞凋亡，进而影响子宫螺旋动脉血管重铸的机制，为子痫前期的早期防治提供理论基础。

Preeclampsia, a complication of pregnancy, which usually presents with hypertension, proteinuria and even multiple organ failure, threatens maternal and fetal health. Inadequate uterine spiral artery remodeling is widely found in the placenta of preeclampsia, characterized by trophoblastic invasion disorders, endothelial cells and vascular smooth muscle cells retained. But, the mechanism is unknown. Our previous study found that transthyretin(TTR) was significantly decreased in the serum of preeclampsia patients, and the TTR level of healthy pregnant women in the first trimester was higher than the nonpregnant persons. In vivo, TTR can bind with the soluble lysosomal associated membrane protein -1 (LAMP-1), causing aggregation of LAMP-1. LAMP-1 is an important component of lysosomal membrane proteins, maintaining the lysosomal membrane stability, reducing the sensitivity of the lysosomal membrane permeability and reducing lysosomal induced cell apoptosis. Our latest studies also show that TTR can reduce the content of membrane LAMP-1 of human umbilical vascular cells. And this research might be helpful in treat preeclampsia, and be of great interest for researchers of female health.