Cited by 51Pregnancy and preeclampsia studiesBirth, Development, and HealthNeonatal and fetal brain pathology

Gene Expression Patterns in the Hypoxic Murine Placenta: A Role in Epigenesis?

Gheorghe, Ciprian P., Mohan, Subburaman, Oberg, Kerby C., Longo, Lawrence D.·2007·Reproductive Sciences

Abstract

Hypoxia has been identified as a major stress or in placental and fetal development. To test the hypothesis that hypoxic stress responses are associated with gene expression changes, the authors measured gene expression in the mouse placenta in response to 48 hours of hypoxia. Embryonic day 15.5 pregnant mice were exposed to 48 hours of hypoxia (10.5% O(2)), after which the Affymetrix Mouse 430A_2.0 array was used to measure gene expression changes in the placenta. The authors observed 171 probe sets, corresponding to 163 genes, that were regulated by hypoxia (P < .01). Ninety genes were upregulated, and 73 were downregulated. The authors functionally annotated the regulated genes and examined overrepresented functional categories. Among the upregulated and downregulated genes, several overrepresented functional categories were observed. Upregulated genes included those involved in metabolism, oxygen transport, proteolysis, cell death, metabolism of reactive oxygen species, and DNA methylation. Genes involved in transcription, cell cycle regulation, and cell structure were downregulated. Microarray analysis has allowed the description of the genetic responses to hypoxia in the mouse placenta. The observation that hypoxia upregulates reactive oxygen species metabolism, in conjunction with DNA methylation enzymes, suggests that hypoxia may contribute to long-term epigenetic changes in stressed fetal tissues and organs.

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Crossref · 10.1177/1933719107302860

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  • In the mouse placenta, vascularity has been shown to be increased in late gestation by 48h of hypoxia, but decreased by longer exposures.

    “In the mouse placenta, vascularity has been shown to be increased in late gestation by 48h of hypoxia, but decreased by longer exposures (133, 212) (Table 3).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [212]

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Authors
Gheorghe, C. P., Mohan, S., Oberg, K. C., & Longo, L. D.
Affiliations
  • Loma Linda University Medical Center (US)
  • Jerry L. Pettis Memorial VA Medical Center (US)
  • Loma Linda University (US)
Corresponding author
Longo, Lawrence D.
Venue
Reproductive Sciences
Published
2007-04
Volume
14
Issue
3
Pages
223-233
ISSN
  • 1933-7191 (ISSN-L)
  • 1933-7205
OpenAlex
W2054958147
Cited by
51
References
46
Citations by year
2026: 1 · 2021: 4 · 2020: 2 · 2019: 4 · 2018: 3 · 2017: 3 · 2016: 3 · 2015: 1 · 2014: 2 · 2013: 4 · 2012: 3
FWCI
5.45
Type
journal article
Language
en
Open access
closed
Locations
  • Reproductive Sciences (publishedVersion)
  • PubMed (publishedVersion)
Funders
Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD-03807, R01HD003807)
Topics
  • Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Neonatal and fetal brain pathology
Keywords
placental hypoxia, gene expression, epigenesis, DNA methylation, reactive oxygen species metabolism, oxygen transport, fetal development, placenta, mouse embryo, hypoxia response genes, cell death
MeSH terms
Animals, Female, Fetal Hypoxia, Placenta, Pregnancy, RNA, Messenger, Polymerase Chain Reaction, Reactive Oxygen Species, Gene Expression Regulation, Developmental, DNA Methylation, Gene Expression Profiling, Epigenesis, Genetic, Mice

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