Cited by 169Birth, Development, and HealthPregnancy and preeclampsia studiesEstrogen and related hormone effects

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Altered Placental Function of 11β-Hydroxysteroid Dehydrogenase 2 Knockout Mice

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Wyrwoll, Caitlin S., Seckl, Jonathan R., Holmes, Megan C.·2009·Endocrinology

DOI 10.1210/en.2008-1100PMC PMC6435187

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Abstract

Fetal glucocorticoid exposure is a key mechanism proposed to underlie prenatal "programming" of adult cardiometabolic and neuropsychiatric disorders. Regulation of fetal glucocorticoid exposure is achieved by the placental glucocorticoid "barrier," which involves glucocorticoid inactivation within the labyrinth zone of the murine placenta by 11beta-hydroxysteroid dehydrogenase 2 (11beta-HSD2). Thus, the absence of placental 11beta-HSD2 may impact on fetal and placental development. The current study investigated transport of amino acids and glucose, key factors required for fetal growth, and vascular development in placentas from 11beta-HSD2(+/+), (+/-), and (-/-) fetuses derived from 11beta-HSD2(+/-) matings. At embryonic d 15 (E15) (term = E19), 11beta-HSD2(-/-) fetal weight was maintained in comparison to 11beta-HSD2(+/+) fetuses. The maintenance of 11beta-HSD2(-/-) fetal weight occurred despite a reduction in placental weight, suggesting that compensatory changes occur in the placenta to maintain function. However, by E18, 11beta-HSD2(-/-) fetal and placental weights were both reduced. Transport studies revealed up-regulation of placental amino acid transport to 11beta-HSD2(-/-) offspring at E15, coinciding with an increase in the expression of the amino acid transporters. Furthermore, at E18, placental glucose transport to 11beta-HSD2(-/-) offspring was markedly reduced, correlating with lower fetal weight and a decrease in glucose transporter 3 expression. Stereological analyses of the labyrinth zone of the placenta revealed that the reduction in placental weight at E18 was associated with restriction of the normal increase in fetal vessel density over the final third of pregnancy. Our data suggest that restriction of fetal growth in 11beta-HSD2(-/-) mice is mediated, at least in part, via altered placental transport of nutrients and reduction in placental vascularization.

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Authors: Wyrwoll, C. S., Seckl, J. R., & Holmes, M. C.
Affiliations: The Queen's Medical Research Institute (GB)
Corresponding author: Wyrwoll, Caitlin S.
ORCID: Wyrwoll, Caitlin S.
Seckl, Jonathan R.
Holmes, Megan C.
Venue: Endocrinology
Publisher: The Endocrine Society
Published: 2008-10-09
Volume: 150
Issue: 3
Pages: 1287-1293
ISSN: 0013-7227 (ISSN-L)
1945-7170
DOI: 10.1210/en.2008-1100
PMC: PMC6435187
OpenAlex: W2165037530
Cited by: 169
References: 37
Citations by year: 2026: 5 · 2025: 5 · 2024: 3 · 2023: 8 · 2022: 13 · 2021: 7 · 2020: 5 · 2019: 8 · 2018: 9 · 2017: 11 · 2016: 16 · 2015: 11 · 2014: 11 · 2013: 12 · 2012: 14
FWCI: 8.99
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Endocrinology (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
UWA Profiles and Research Repository (UWA) (submittedVersion)
Funders: Wellcome Trust (079009)
Topics: Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
Keywords: 11β-hydroxysteroid dehydrogenase type 2, fetal glucocorticoid exposure, fetal growth restriction, amino acid transport, glucose transport, GLUT3, placental vascularization, placental labyrinth zone, fetal programming, knockout mice
MeSH terms: Amino Acids, Animals, Biological Transport, Blood Glucose, Embryo, Mammalian, Female, Fetal Growth Retardation, Glucose, Male, Maternal-Fetal Exchange, Mice, Inbred C57BL, Organ Size, Placenta, Placenta Diseases, Pregnancy, Mice, Knockout, Fetal Weight, Placental Circulation, 11-beta-Hydroxysteroid Dehydrogenase Type 2, Mice

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Altered Placental Function of 11β-Hydroxysteroid Dehydrogenase 2 Knockout Mice

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