EPAS1 expression contributes to maintenance of the primordial follicle pool in the mouse ovary

© 2024. The Author(s)..

Oxygen availability can have profound effects on cell fate decisions and survival, in part by regulating expression of hypoxia-inducible factors (HIFs). In the ovary, HIF expression has been characterised in granulosa cells, however, any requirement in oocytes remains relatively undefined. Here we developed a Hif2a/Epas1 germline-specific knockout mouse line in which females were fertile, however produced 40% fewer pups than controls. No defects in follicle development were detected, and quality of MII oocytes was normal, as per assessments of viability, intracellular reactive oxygen species, and spindle parameters. However, a significant diminishment of the primordial follicle pool was evident in cKO females that was attributed to accelerated follicle loss from postnatal day 6 onwards, potentially via disruption of the autophagy pathway. These data demonstrate the importance of HIF signalling in oocytes, particularly at the primordial follicle stage, and lend to the importance of controlling oxygen tension in the development of in vitro growth and maturation approaches for assisted reproduction.

Medienart:

E-Artikel

Erscheinungsjahr:

2024

Erschienen:

2024

Enthalten in:

Zur Gesamtaufnahme - volume:14

Enthalten in:

Scientific reports - 14(2024), 1 vom: 16. Apr., Seite 8770

Sprache:

Englisch

Beteiligte Personen:

Martin, Jacinta H [VerfasserIn]
Bernstein, Ilana R [VerfasserIn]
Lyons, Jess M [VerfasserIn]
Brady, Ariel R [VerfasserIn]
Mabotuwana, Nishani S [VerfasserIn]
Stanger, Simone J [VerfasserIn]
De Oliveira, Camila Salum [VerfasserIn]
Damyanova, Katerina B [VerfasserIn]
Nixon, Brett [VerfasserIn]
Lord, Tessa [VerfasserIn]

Links:

Volltext

Themen:

1B37H0967P
Autophagy
EPAS1
Endothelial PAS domain-containing protein 1
Folliculogenesis
HIF
Hypoxia
Journal Article
Oocyte
Oxygen
Primordial follicle
S88TT14065

Anmerkungen:

Date Completed 18.04.2024

Date Revised 25.04.2024

published: Electronic

Citation Status MEDLINE

doi:

10.1038/s41598-024-59382-z

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM371166810