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Cited by 86Birth, Development, and HealthPregnancy and preeclampsia studiesPrenatal Substance Exposure Effects

Sex specific changes in placental growth and MAPK following short term maternal dexamethasone exposure in the mouse

Cuffe, J.S.M., Dickinson, H., Simmons, D.G., Moritz, K.M.·2011·Placenta
DOI 10.1016/j.placenta.2011.09.009
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Abstract

Objectives Maternal glucocorticoid (GC) exposure during pregnancy can alter fetal development and program the onset of disease in adult offspring. The placenta helps protect the fetus from excess GC exposure but is itself susceptible to maternal insults and may be involved in sex dependant regulation of fetal programming. This study aimed to investigate the effects of maternal GC exposure on the developing placenta.Study design and main outcome measures Pregnant mice were treated with dexamethasone (DEX-1 μg/kg/h) or saline (SAL) for 60 h via minipump beginning at E12.5. Placentas were collected at E14.5 and E17.5 and the expression of growth factors and placental transporters examined by real-time PCR and/or Western blot. Histological analysis was performed to assess for morphological changes.Results At E14.5, DEX exposed male and female fetuses had a lower weight compared to SAL animals but placental weight was lower in females only. Hsd11b2 and Vegfa gene expression was increased and MAPK1 protein expression decreased in the placentas of females only. At E17.5 placental and fetal body weights were similar and differences in MAPK were no longer present although HSD11B2 protein was elevated in placentas of DEX females. Levels of glucose or amino acid transporters were unaffected.Conclusions Results suggest sex specific responses to maternal GCs within the placenta. Decreased levels of MAPK protein in placentas of female fetuses suggest alterations in the MAPK pathway may contribute to the lower placental weights in this sex. This may contribute towards sex specific fetal programming of adult disease.

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Crossref · 10.1016/j.placenta.2011.09.009

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  • Sex-dependent differences in gene expression are likely to underlie the contrasting placental responses observed following exposure to high-fat/low-fat diets, glucocorticoids, or hypoxia in mice.

    “Nonetheless, sex-dependent differences in gene expression are likely to underlie the contrasting placental responses observed following exposure to high-fat/low-fat diets (202, 356), glucocorticoids (132), or hypoxia (133, 363) in mice.”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [132]

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Authors
Cuffe, J. S. M., Dickinson, H., Simmons, D. G., & Moritz, K. M.
Affiliations
  • The University of Queensland (AU)
  • Monash Institute of Medical Research (AU)
Corresponding author
Moritz, K.M.
ORCID
Venue
Placenta
Publisher
Elsevier BV
Published
2011-12
Volume
32
Issue
12
Pages
981-989
ISSN
0143-4004 (ISSN-L)
DOI
10.1016/j.placenta.2011.09.009
OpenAlex
W2123883807
Cited by
86
References
41
Citations by year
2026: 3 · 2025: 1 · 2024: 2 · 2023: 3 · 2022: 4 · 2021: 5 · 2020: 4 · 2019: 5 · 2018: 9 · 2017: 11 · 2016: 12 · 2015: 11 · 2014: 4 · 2013: 5 · 2012: 7
FWCI
4.71
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Placenta (publishedVersion)
  • PubMed (publishedVersion)
  • Griffith Research Online (submittedVersion)
Funders
  • National Health and Medical Research Council
  • Australian Research Council
  • University of Queensland
Topics
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
Keywords
maternal glucocorticoid exposure, dexamethasone, placental development, sex differences, fetal programming, MAPK1, 11β-hydroxysteroid dehydrogenase type 2, VEGF-A, placental weight, placental transporters, fetal growth restriction, placental histology
MeSH terms
Animals, Dexamethasone, Female, Fetus, Male, Mice, Inbred C57BL, Organ Size, Placenta, Placentation, Pregnancy, Receptors, Glucocorticoid, Sex Factors, Gene Expression Regulation, Developmental, Mitogen-Activated Protein Kinase 1, Vascular Endothelial Growth Factor A, 11-beta-Hydroxysteroid Dehydrogenase Type 2, Mice

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