Silencing of maternal hepatic glucocorticoid receptor is essential for normal fetal development in mice.
Journal
Communications biology
ISSN: 2399-3642
Titre abrégé: Commun Biol
Pays: England
ID NLM: 101719179
Informations de publication
Date de publication:
2019
2019
Historique:
received:
28
08
2018
accepted:
17
01
2019
entrez:
27
3
2019
pubmed:
27
3
2019
medline:
27
3
2019
Statut:
epublish
Résumé
Excessive or chronic stress can lead to a variety of diseases due to aberrant activation of the glucocorticoid receptor (GR), a ligand activated transcription factor. Pregnancy represents a particular window of sensitivity in which excessive stress can have adverse outcomes, particularly on the developing fetus. Here we show maternal hepatic stress hormone responsiveness is diminished via epigenetic silencing of the glucocorticoid receptor during pregnancy. Provocatively, reinstallation of GR to hepatocytes during pregnancy by adeno-associated viral transduction dysregulates genes involved in proliferation, resulting in impaired pregnancy-induced hepatomegaly. Disruption of the maternal hepatic adaptation to pregnancy results in in utero growth restriction (IUGR). These data demonstrate pregnancy antagonizes the liver-specific effects of stress hormone signaling in the maternal compartment to ultimately support the healthy development of embryos.
Identifiants
pubmed: 30911679
doi: 10.1038/s42003-019-0344-3
pii: 344
pmc: PMC6420645
doi:
Substances chimiques
Glucocorticoids
0
Receptors, Glucocorticoid
0
Types de publication
Journal Article
Research Support, N.I.H., Intramural
Langues
eng
Pagination
104Subventions
Organisme : Intramural NIH HHS
ID : ZIA ES090057
Pays : United States
Déclaration de conflit d'intérêts
The authors declare no competing interests.
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