PDCD4 deficiency improved 4-vinylcyclohexene dioxide-induced mouse premature ovarian insufficiency.
Reprod Biomed Online
; 48(4): 103685, 2024 Apr.
Article
em En
| MEDLINE
| ID: mdl-38324980
ABSTRACT
RESEARCH QUESTION What role does programmed cell death 4 (PDCD4) play in premature ovarian insufficiency (POI)? DESIGN:
A PDCD4 gene knockout (PDCD4-/-) mouse model was constructed, a POI mouse model was established similar to human POI with 4-vinylcyclohexene dioxide (VCD), a PDCD4-overexpressed adenovirus was designed and the regulatory role in POI in vitro and in vivo was investigated.RESULTS:
PDCD4 expression was significantly increased in the ovarian granulosa cells of patients with POI (P ≤ 0.002 protein and mRNA) and mice with VCD-induced POI (P < 0.001 protein expression in both mouse ovaries and granulosa cells). In POI-induced mice model, PDCD4 knockouts significantly increased anti-Müllerian hormone, oestrodiol and numbers of developing follicles, and the PI3K-AKT-Bcl2/Bax signalling pathway is involved in it.CONCLUSION:
The expression and regulation of PDCD4 significantly affects the POI pathology in a mouse model. This effect is closely related to the regulation of Bcl2/Bax and the activation of the PI3K-AKT signalling pathway.Palavras-chave
Texto completo:
1
Bases de dados:
MEDLINE
Assunto principal:
Insuficiência Ovariana Primária
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Cicloexenos
Limite:
Animals
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Female
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Humans
Idioma:
En
Revista:
Reprod Biomed Online
Assunto da revista:
MEDICINA REPRODUTIVA
Ano de publicação:
2024
Tipo de documento:
Article