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Crossing mice deficient in eNOS with placental-specific Igf2 knockout mice: A new model of fetal growth restriction

We tested the hypothesis that crossing two mouse models of fetal growth restriction (FGR) of differing phenotype would induce more severe FGR than either model alone. Female endothelial nitric oxide synthase knockout mice (eNOS(−/−)) were mated with placental-specific Igf2 knockout males (P0). Resul...

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Detalles Bibliográficos
Autores principales: Dilworth, M.R., Kusinski, L.C., Baker, B.C., Renshall, L.J., Baker, P.N., Greenwood, S.L., Wareing, M., Sibley, C.P.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: W.B. Saunders 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3556783/
https://www.ncbi.nlm.nih.gov/pubmed/23099110
http://dx.doi.org/10.1016/j.placenta.2012.09.012
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author Dilworth, M.R.
Kusinski, L.C.
Baker, B.C.
Renshall, L.J.
Baker, P.N.
Greenwood, S.L.
Wareing, M.
Sibley, C.P.
author_facet Dilworth, M.R.
Kusinski, L.C.
Baker, B.C.
Renshall, L.J.
Baker, P.N.
Greenwood, S.L.
Wareing, M.
Sibley, C.P.
author_sort Dilworth, M.R.
collection PubMed
description We tested the hypothesis that crossing two mouse models of fetal growth restriction (FGR) of differing phenotype would induce more severe FGR than either model alone. Female endothelial nitric oxide synthase knockout mice (eNOS(−/−)) were mated with placental-specific Igf2 knockout males (P0). Resultant fetuses were no more growth restricted than those with P0 deletion alone. However, P0 deletion attenuated the reduced placental system A amino acid transporter activity previously observed in eNOS(−/−) mice. Manipulating maternal and fetal genotypes provides a means to compare maternal and fetal regulation of fetal growth.
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spelling pubmed-35567832013-01-28 Crossing mice deficient in eNOS with placental-specific Igf2 knockout mice: A new model of fetal growth restriction Dilworth, M.R. Kusinski, L.C. Baker, B.C. Renshall, L.J. Baker, P.N. Greenwood, S.L. Wareing, M. Sibley, C.P. Placenta Short Communication We tested the hypothesis that crossing two mouse models of fetal growth restriction (FGR) of differing phenotype would induce more severe FGR than either model alone. Female endothelial nitric oxide synthase knockout mice (eNOS(−/−)) were mated with placental-specific Igf2 knockout males (P0). Resultant fetuses were no more growth restricted than those with P0 deletion alone. However, P0 deletion attenuated the reduced placental system A amino acid transporter activity previously observed in eNOS(−/−) mice. Manipulating maternal and fetal genotypes provides a means to compare maternal and fetal regulation of fetal growth. W.B. Saunders 2012-12 /pmc/articles/PMC3556783/ /pubmed/23099110 http://dx.doi.org/10.1016/j.placenta.2012.09.012 Text en © 2012 Elsevier Ltd. https://creativecommons.org/licenses/by/3.0/ Open Access under CC BY 3.0 (https://creativecommons.org/licenses/by/3.0/) license
spellingShingle Short Communication
Dilworth, M.R.
Kusinski, L.C.
Baker, B.C.
Renshall, L.J.
Baker, P.N.
Greenwood, S.L.
Wareing, M.
Sibley, C.P.
Crossing mice deficient in eNOS with placental-specific Igf2 knockout mice: A new model of fetal growth restriction
title Crossing mice deficient in eNOS with placental-specific Igf2 knockout mice: A new model of fetal growth restriction
title_full Crossing mice deficient in eNOS with placental-specific Igf2 knockout mice: A new model of fetal growth restriction
title_fullStr Crossing mice deficient in eNOS with placental-specific Igf2 knockout mice: A new model of fetal growth restriction
title_full_unstemmed Crossing mice deficient in eNOS with placental-specific Igf2 knockout mice: A new model of fetal growth restriction
title_short Crossing mice deficient in eNOS with placental-specific Igf2 knockout mice: A new model of fetal growth restriction
title_sort crossing mice deficient in enos with placental-specific igf2 knockout mice: a new model of fetal growth restriction
topic Short Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3556783/
https://www.ncbi.nlm.nih.gov/pubmed/23099110
http://dx.doi.org/10.1016/j.placenta.2012.09.012
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