Regulatory roles for the functional network of placenta on maintenance of homeostasis during pregnancy

为了阐明正常妊娠期间胎盘功能网络对维持稳态的调节作用，我使用全基因组表达谱在分子水平上表征妊娠小鼠的胎盘。代谢和新血管生成相关基因的表达水平的动态变化进行了鉴定。另一方面，在人类中，妊娠高血压综合征（PIH）被认为是由于妊娠稳态的破坏。在本研究中，我发现，妊娠相关性高血压（PAH）小鼠，这是以前在我们的实验室，表现出的病理条件，包括妊高征的标准。此外，通过评估PAH小鼠中抗高血压药物的改善特性，我证明了阻断血管加压素血管紧张素II的受体AT 1对预防这种妊娠相关疾病的有效性。

To clarify the regulatory roles for the functional network of placenta on maintenance of homeostasis during normal pregnancy, I used full genome expression profiling to characterize the placenta of pregnant mice at a molecular level. The dynamic changes in the expression levels of metabolism- and neoangiogenesis-related genes were identified. On the other hand, in human, it is assumed that pregnancy-induced hypertension (PIH) is resulting from the breakdown of the pregnancy homeostasis. In this study, I showed that pregnancy-associated hypertensive (PAH) mice, which were previously generated in our laboratory, exhibited the pathological condition including the criteria of PIH. In addition, by evaluating the ameliorative properties of the antihypertensive drugs in PAH mice, I demonstrated the effectiveness of blockade of AT1, a receptor of vasopressor angiotensin II, on prevention of this pregnancy-related disease.