Oviductal Retention of Embryos in Female Mice Lacking Estrogen Receptor α in the Isthmus and the Uterus.
embryo transport
estrogen receptor α
oviduct
pituitary gland
uterus
Journal
Endocrinology
ISSN: 1945-7170
Titre abrégé: Endocrinology
Pays: United States
ID NLM: 0375040
Informations de publication
Date de publication:
01 02 2020
01 02 2020
Historique:
revised:
04
06
2019
accepted:
16
12
2019
pubmed:
29
12
2019
medline:
16
7
2020
entrez:
29
12
2019
Statut:
ppublish
Résumé
Estrogen receptor α (ESR1; encoded by Esr1) is a crucial nuclear transcription factor for female reproduction and is expressed throughout the female reproductive tract. To assess the function of ESR1 in reproductive tissues without confounding effects from a potential developmental defect arising from global deletion of ESR1, we generated a mouse model in which Esr1 was specifically ablated during postnatal development. To accomplish this, a progesterone receptor Cre line (PgrCre) was bred with Esr1f/f mice to create conditional knockout of Esr1 in reproductive tissues (called PgrCreEsr1KO mice) beginning around 6 days after birth. In the PgrCreEsr1KO oviduct, ESR1 was most efficiently ablated in the isthmic region. We found that at 3.5 days post coitus (dpc), embryos were retrieved from the uterus in control littermates while all embryos were retained in the PgrCreEsr1KO oviduct. Additionally, serum progesterone (P4) levels were significantly lower in PgrCreEsr1KO compared to controls at 3.5 dpc. This finding suggests that expression of ESR1 in the isthmus and normal P4 levels allow for successful embryo transport from the oviduct to the uterus. Therefore, alterations in oviductal isthmus ESR1 signaling and circulating P4 levels could be related to female infertility conditions such as tubal pregnancy.
Identifiants
pubmed: 31883000
pii: 5688715
doi: 10.1210/endocr/bqz033
pmc: PMC7295936
pii:
doi:
Substances chimiques
Estrogen Receptor alpha
0
Progesterone
4G7DS2Q64Y
Estradiol
4TI98Z838E
Luteinizing Hormone
9002-67-9
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NICHD NIH HHS
ID : R01 HD097087
Pays : United States
Organisme : NICHD NIH HHS
ID : R01 HD042311
Pays : United States
Informations de copyright
© Endocrine Society 2019. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
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