1. The atrial natriuretic peptide (ANP) knockout mouse does not exhibit the phenotypic features of pre-eclampsia or demonstrate fetal growth restriction
- Author
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Finn-Sell, Sarah L., Renshall, Lewis J., Cowley, Elizabeth J., Dilworth, Mark R., Wareing, Mark, Greenwood, Susan L., Sibley, Colin P., and Cottrell, Elizabeth C.
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Mice, Knockout ,Fetal Growth Retardation ,Mouse ,Short Communication ,Placenta ,Fetal growth restriction ,Blood Pressure ,Disease Models, Animal ,Mice ,Reproductive Medicine ,Pregnancy ,embryonic structures ,Obstetrics and Gynaecology ,cardiovascular system ,Animals ,Female ,Atrial natriuretic peptide ,Pre-eclampsia ,Atrial Natriuretic Factor ,reproductive and urinary physiology ,hormones, hormone substitutes, and hormone antagonists ,circulatory and respiratory physiology ,Developmental Biology - Abstract
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., Highlights • Mouse models of pre-eclampsia and fetal growth restriction are needed to test potential therapies. • ANP knockout mice have previously been identified as a potential model of pre-eclampsia. • We find that these mice do not exhibit pregnancy-associated hypertension, or fetal growth restriction. • ANP knockout mice do not provide a robust model of pre-eclampsia or fetal growth restriction.
- Published
- 2016
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