Uteroplacental ischemia results in proteinuric hypertension and elevated sFLT-1
Uteroplacental ischemia results in proteinuric hypertension and elevated sFLT-1
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DOI：
10.1038/sj.ki.5002175
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发表时间：
2007-05-01
影响因子：
19.6
通讯作者：
Hennessy, A.
中科院分区：
文献类型：
--
作者：
Makris, A.;Thornton, C.;Hennessy, A.
先兆子痫是一种妊娠并发症，对母亲和胎儿具有显著的发病率和死亡率。推测胎盘缺氧在临床综合征中具有致病作用。此外，可溶性fms样酪氨酸激酶1（sFLT-1）已被证明在先兆子痫的母体综合征中发挥作用。我们研究了非人灵长类动物子宫胎盘缺血（UPI）、先兆子痫的母体临床综合征和sFLT-1之间的关系。在怀孕的非人灵长类动物中诱导UPI导致类似于人先兆子痫的临床实体的发展。这通过血压升高、蛋白尿的发展和与人类先兆子痫相同的肾组织学变化来说明。观察到胎盘和外周血单核细胞sFLT-1 mRNA表达显著升高，转化为循环sFLT-1显著升高。因此，该序列表明胎盘灌注的致病性减少导致先兆子痫的母体综合征的发展和循环sFLT-1的增加，其来源于胎盘和胎盘外来源。
Preeclampsia is a complication of pregnancy with significant morbidity and mortality for the mother and the fetus. Presumptions are made that placental hypoxia has a causative role in the clinical syndrome. Furthermore, soluble fms-like tyrosine kinase 1 (sFLT-1) has been shown to have a role in the maternal syndrome of preeclampsia. We investigated the relationship between uteroplacental ischemia (UPI), the maternal clinical syndrome of preeclampsia and sFLT-1 in non-human primates. The induction of UPI in a pregnant non- human primate resulted in the development of a clinical entity analogous to human preeclampsia. This was illustrated by the increase in blood pressure, development of proteinuria, and renal histological changes identical to human preeclampsia. A significant elevation in the placental and peripheral blood mononuclear cell sFLT-1 mRNA expression was noted, translating to a significant elevation in circulating sFLT-1. Thus, this sequence suggests that a pathogenic reduction in placental perfusion results in the development of the maternal syndrome of preeclampsia and an increase in circulating sFLT-1, which is derived both from placental and extra-placental sources.