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

Placenta. 2012 Dec;33(12):1052-4. doi: 10.1016/j.placenta.2012.09.012. Epub 2012 Oct 23.

Abstract

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.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Transport System A / metabolism
  • Animals
  • Crosses, Genetic
  • Disease Models, Animal*
  • Female
  • Fetal Growth Retardation / enzymology
  • Fetal Growth Retardation / metabolism*
  • Fetal Growth Retardation / pathology
  • Fetal Growth Retardation / physiopathology
  • Fetal Weight
  • Heterozygote
  • Homozygote
  • Insulin-Like Growth Factor II / genetics
  • Insulin-Like Growth Factor II / metabolism*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Nitric Oxide Synthase Type III / genetics
  • Nitric Oxide Synthase Type III / metabolism*
  • Organ Size
  • Organ Specificity
  • Placenta / enzymology
  • Placenta / metabolism*
  • Placenta / pathology
  • Pregnancy
  • Severity of Illness Index

Substances

  • Amino Acid Transport System A
  • IGF2 protein, mouse
  • Insulin-Like Growth Factor II
  • Nitric Oxide Synthase Type III
  • Nos3 protein, mouse