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首页> 外文期刊>Biochimica et biophysica acta: BBA: International journal of biochemistry, biophysics and molecular biololgy. Proteins and Proteomics >Involvement of placental peptidases associated with renin-angiotensin systems in preeclampsia
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Involvement of placental peptidases associated with renin-angiotensin systems in preeclampsia

机译：子痫前期与肾素-血管紧张素系统相关的胎盘肽酶的参与

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Preeclampsia is characterized by pregnancy-induced hypertension accompanied with protein urea and generalized edema. Preeclampsia develops during the second half of pregnancy and resolves postpartum promptly, implicating the placenta as a primary cause in the disorder. Normal pregnancy is associated with reductions in arterial pressure and attenuated pressor response to exogenous infused angiotensin II (ANG II). In contrast, women with preeclampsia show the similar sensitivity to the pressor effect of ANG II as do non-pregnant women. To elucidate the involvement of placental peptidases associated with renin-angiotensin systems, we determined the localization of angiotensin converting enzyme (ACE) and aminopeptidase A (AP-A), ANG II degrading enzyme, in the placenta and compared the expression of mRNA and protein in uncomplicated and preeclamptic placenta. In addition, AP-A expression in trophoblastic cells treated with ANG II and ACE expression in HUVECs under hypoxic condition were analyzed, respectively. The expression of both peptidases in the preeclamptic placenta was significantly higher than those from uncomplicated. ACE was primarily localized to venous endothelial cells of stern villous whereas AP-A expression was recognized in the trophoblast and pericytes of fetal arterioles and venules within stern villous. Hypoxia induced ACE expression in HUVECs while both hypoxia and ANG II evoked AP-A expression in trophoblast. These results suggested that hypoxic condition in preeclampsia induces ACE activation in feto-placental unit to maintain the fetal hemodynamics and placental AP-A plays a role as a component of the barrier of ANG II between mother and fetus. (c) 2005 Elsevier B.V. All rights reserved.
机译：子痫前期的特征是妊娠引起的高血压，伴有蛋白尿素和全身性水肿。子痫前期在妊娠的后半期发展，并在产后迅速消退，这说明胎盘是该疾病的主要原因。正常妊娠与动脉压降低和对外源性输注血管紧张素II（ANG II）的升压反应减弱有关。相比之下，先兆子痫的妇女对ANG II的升压作用的敏感性与未怀孕的妇女相似。为了阐明与肾素-血管紧张素系统相关的胎盘肽酶的参与，我们确定了胎盘中血管紧张素转化酶（ACE）和氨肽酶A（AP-A），ANG II降解酶的定位，并比较了mRNA和蛋白的表达在简单和先兆子痫的胎盘中。另外，分别分析了在缺氧条件下用ANG II处理的滋养细胞中的AP-A表达和在HUVEC中的ACE表达。子痫前期胎盘中两种肽酶的表达均显着高于单纯性胎盘。 ACE主要位于尾部绒毛的静脉内皮细胞中，而AP-A表达在尾部绒毛中的胎儿小动脉和小静脉的滋养层和周细胞中被识别。低氧诱导HUVECs ACE表达，而低氧和ANG II都引起滋养细胞AP-A表达。这些结果表明先兆子痫的低氧条件诱导胎儿胎盘单元中的ACE活化以维持胎儿的血流动力学，而胎盘AP-A充当母亲与胎儿之间ANG II屏障的组成部分。 （c）2005 Elsevier B.V.保留所有权利。

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