Cited by 179Genetic Syndromes and ImprintingBirth, Development, and HealthPregnancy and preeclampsia studies

Regulation of Placental Efficiency for Nutrient Transport by Imprinted Genes

Angiolini, E., Fowden, A., Coan, P., Sandovici, I., Smith, P., Dean, W., Burton, G., Tycko, B. +3 more·2006·Placenta

Abstract

Intrauterine growth and development can impact upon the long-term health of an individual. The fetus is dependent upon the placenta for its supply of nutrients and oxygen from the mother. In turn, the functional capacity of the placenta to supply that demand is under the control of the fetal and maternal genomes. Recent evidence suggests that imprinted genes, a class of genes found in placental mammals whose expression depends on their parental origin, have multiple roles in the placenta. The imprinted genes regulate the growth and transport capacity of the placenta, thereby controlling the supply of nutrients. They may also regulate the growth rate of fetal tissues directly, thereby controlling nutrient demand by the fetus. Recent studies using mice with deletions or disruption of imprinted genes with an altered balance between placental and fetal growth and changes in placental efficiency are indicative of feto-placental signalling of fetal nutrient demand. We propose that signalling mechanisms involving growth demand signals and nutrient transporters are likely to occur and are important for fine tuning normal fetal growth.

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Crossref · 10.1016/j.placenta.2005.12.008

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  • The reduced passive permeability, nutrient transport and/or transporter expression of these mutant placentas may reflect the dominance of maternal signals that constrain maternal-fetal resource allocation in the face of the increased drain posed by the overgrown conceptuses in late gestation.

    “The reduced passive permeability, nutrient transport and/or transporter expression of these mutant placentas may reflect the dominance of maternal signals that constrain maternal-fetal resource allocation in the face of the increased drain posed by the overgrown conceptuses in late gestation (14,15).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [15]

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Authors
Angiolini, E., Fowden, A., Coan, P., Sandovici, I., Smith, P., Dean, W., Burton, G., Tycko, B., Reik, W., Sibley, C., & Constância, M.
Affiliations
  • Babraham Institute (GB)
  • University of Cambridge (GB)
  • Columbia University (US)
  • University of Manchester (GB)
Corresponding author
Angiolini, E.
Venue
Placenta
Publisher
Elsevier BV
Published
2006-04
Volume
27
Pages
98-102
ISSN
0143-4004 (ISSN-L)
OpenAlex
W2054923768
Cited by
179
References
31
Citations by year
2026: 2 · 2025: 5 · 2024: 2 · 2023: 4 · 2022: 6 · 2021: 10 · 2020: 6 · 2019: 7 · 2018: 6 · 2017: 7 · 2016: 11 · 2015: 9 · 2014: 7 · 2013: 10 · 2012: 22
FWCI
5.26
Type
journal article
Language
en
Open access
closed
Locations
  • Placenta (publishedVersion)
  • PubMed (publishedVersion)
Funders
Biotechnology and Biological Sciences Research Council (BB/B50118X/1, S18929)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Syndromes and Imprinting
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
Keywords
genomic imprinting, imprinted genes, placental efficiency, nutrient transport, fetal growth, nutrient transporters, placental development
MeSH terms
Animals, Female, Placenta, Pregnancy, RNA-Binding Proteins, Mice, Knockout, Genomic Imprinting, Gene Expression Regulation, Developmental, Fetal Development, Mice

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