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Updated: May 30, 2026

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System A activity and vascular function in the placental-specific Igf2 knockout mouse.

L C Kusinski1, M R Dilworth, P N Baker

  • 1Maternal and Fetal Health Research Centre, School of Biomedicine, Manchester Academic Health Science Centre, The University of Manchester, St Mary's Hospital, Manchester M13 9WL, UK.

Placenta
|August 20, 2011
PubMed
Summary

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Insulin-like growth factor 2 (Igf2) P0 knockout mice show increased placental nutrient transport early in pregnancy, but this is not sustained, leading to fetal growth restriction (FGR). This FGR is linked to reduced placental nutrient exchange, not vascular issues.

Area of Science:

  • Reproductive biology
  • Developmental biology
  • Maternal-fetal medicine

Background:

  • The placental-specific P0 transcript of insulin-like growth factor 2 (Igf2) is crucial for placental development.
  • Igf2 P0 knockout (P0) fetuses exhibit fetal growth restriction (FGR) by late gestation.
  • Early pregnancy in P0 fetuses shows increased maternofetal amino acid transport, but this adaptation is transient.

Purpose of the Study:

  • To investigate the role of System A amino acid transporter activity in the transient increase of nutrient transfer in P0 mice.
  • To determine if altered uteroplacental vascular function contributes to FGR in P0 mice.
  • To test the hypothesis that FGR in P0 mice is primarily due to altered nutrient transport, not vascular dysfunction.

Main Methods:

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  • Isolation of placental plasma membrane vesicles from P0 and wild-type (WT) fetuses at embryonic days 16 (E16) and E19.
  • Measurement of System A amino acid transporter activity via sodium-dependent (14)C-methylaminoisobutyric acid ((14)C-MeAIB) uptake.
  • Assessment of uterine artery vascular reactivity using wire myography to measure agonist-induced responses.

    • Main Results:

    • System A amino acid transporter activity was significantly higher in P0 placentas compared to WT at E16.
    • By E19, (14)C-MeAIB uptake was similar between P0 and WT placentas.
    • Uterine artery vascular reactivity showed no significant differences between P0 and WT groups.

    Conclusions:

    • System A activity in the syncytiotrophoblast layer II mediates the observed adaptations in transplacental amino acid flux in P0 mice.
    • The transient nature of enhanced nutrient transport capacity contributes to FGR.
    • Unaltered uterine artery vascular function indicates that FGR in P0 fetuses is primarily caused by impaired placental nutrient exchange capacity.