The DOI matches its Crossref record; 36 of the 37 references it cites were found in a registry or an index.
Altered Placental Function of 11β-Hydroxysteroid Dehydrogenase 2 Knockout Mice
Open accessAbstract
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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“Furthermore, when placental growth is restricted by glucocorticoid overexposure in the 11βHsd2-null mutant, there is upregulation of placental amino acid transfer and transporter expression in association with maintained fetal growth for the first 15 days of gestation (587).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [587]
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“However, this upregulation is not maintained into late gestation, probably due to the decreased fetal demand associated with the direct growth inhibitory effects of excess glucocorticoids on fetal tissues late in gestation (191, 587).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [587]
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Cites
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11β-hydroxysteroid dehydrogenases: Intracellular gate-keepers of tissue glucocorticoid action
Chapman, K., Holmes, M., & Seckl, J. (2013) · Physiological Reviews · doi:10.1152/physrev.00020.2012 · Cited by 887
Self-citationGlucocorticoids, prenatal stress and the programming of disease
Harris, A., & Seckl, J. (2011) · Hormones and Behavior · doi:10.1016/j.yhbeh.2010.06.007 · Cited by 871
Self-citationPlacental Origins of Chronic Disease
Burton, G. J., Fowden, A. L., & Thornburg, K. L. (2016) · Physiological Reviews · doi:10.1152/physrev.00029.2015 · Cited by 717
Prenatal stress, glucocorticoids and the programming of adult disease
Cottrell, E. C. (2009) · Frontiers in Behavioral Neuroscience · doi:10.3389/neuro.08.019.2009 · Cited by 640
Placental efficiency and adaptation: endocrine regulation
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Metadata
- Authors
- Wyrwoll, C. S., Seckl, J. R., & Holmes, M. C.
- Affiliations
- The Queen's Medical Research Institute (GB)
- Corresponding author
- Wyrwoll, Caitlin S.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2008-10-09
- Volume
- 150
- Issue
- 3
- Pages
- 1287-1293
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- 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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