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The atrial natriuretic peptide (ANP) knockout mouse does not exhibit the phenotypic features of pre-eclampsia or demonstrate fetal growth restriction

机译:心钠素基因敲除小鼠没有表现出先兆子痫的表型特征或表现出胎儿生长受限

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摘要

The ANP knockout mouse is reported to exhibit pregnancy-associated hypertension, proteinuria and impaired placental trophoblast invasion and spiral artery remodeling, key features of pre-eclampsia (PE). We hypothesized that these mice may provide a relevant model of human PE with associated fetal growth restriction (FGR). Here, we investigated pregnancies of ANP wild type (ANP+/+), heterozygous (ANP+/-) and knockout (ANP−/-) mice. Maternal blood pressure did not differ between genotypes (E12.5, E17.5), and fetal weight (E18.5) was unaffected. Placental weight was greater in ANP−/− versus ANP+/+ mice. Therefore, in our hands, the ANP model does not express phenotypic features of PE with FGR.
机译:据报道,ANP基因敲除小鼠表现出与妊娠相关的高血压,蛋白尿和胎盘滋养细胞侵袭和螺旋动脉重构受损,这是先兆子痫(PE)的主要特征。我们假设这些小鼠可能提供具有相关胎儿生长限制(FGR)的人类PE的相关模型。在这里,我们调查了ANP野生型(ANP + / + ),杂合子(ANP +/- )和敲除(ANP -/-)的怀孕>)小鼠。孕妇血压在基因型(E12.5,E17.5)之间没有差异,胎儿体重(E18.5)不受影响。与ANP + / + 小鼠相比,ANP -/-小鼠的胎盘重量更大。因此,在我们手中,ANP模型无法表达具有FGR的PE的表型特征。

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