Development and analysis of a mouse model of preeclampsia using transient in vivo gene transfer system

近年来，“两步理论”作为先兆子痫的病理状态受到了很多关注，具体地说，由于妊娠早期绒毛膜对子宫的侵袭不足而导致的胎盘灌注减少被假定为根本原因，而母体系统性内皮功能障碍是由于胎盘缺氧状态而导致的一些过度表达的血管生成因子抑制剂引起的。本研究将调控绒毛膜浸润的相关因子TIMP-3在着床窗期转移到子宫腔中，成功地建立了子痫前期小鼠模型。

Recently, "Two Step Theory" has received a lot of attention as pathological condition of preeclampsia, concretely speaking, reduced placental perfusion due to insufficient chorionic invasion to the uterus at early pregnancy is postulated as the root cause and maternal systemic endothelial dysfunction is induced by some over-expressed inhibitor of angiogenesis factor due to hypoxic status at placenta. In this research, we transferred TIMP-3 which is known as related factor of regulation of chorionic invasion to the decidua into the uterine cavity during implantation window, thus we successfully developed a mouse of preeclampsia.