PI3K/AKT/mTOR通路
毛囊
生物
卵泡
卵泡发生
磷酸酶
细胞凋亡
男科
内科学
污渍
半胱氨酸蛋白酶3
内分泌学
细胞生物学
卵巢
信号转导
磷酸化
胚胎发生
医学
程序性细胞死亡
生物化学
胚胎
基因
作者
Shanshan Zhou,Yueyue Xi,Yingying Chen,Tong Wu,Wei Yan,Milu Li,Meng Wu,Aiyue Luo,Wei Shen,Xiang Tang,Shixuan Wang
标识
DOI:10.1016/j.rbmo.2021.05.007
摘要
What role does wild-type p53-induced phosphatase 1 (WIP1) play in the regulation of primordial follicle development?WIP1 expression was detected in the ovaries of mice of different ages by western blotting and immunohistochemical staining. Three-day-old neonatal mouse ovaries were cultured in vitro with or without the WIP1 inhibitor GSK2830371 (10 μM) for 4 days. Ovarian morphology, follicle growth and follicle classification were analysed and the PI3K-AKT-mTOR signal pathway and the WIP1-p53-related mitochondrial apoptosis pathway evaluated.WIP1 expression was downregulated with age. Primordial follicles were significantly decreased in the GSK2830371-treated group, without a significant increase in growing follicles. The ratio of growing follicles to primordial follicles was not significantly different between the control and GSK2830371 groups, and no significant variation was observed in the PI3K-AKT-mTOR signal pathway. The inhibition of WIP1 phosphatase accelerated primordial follicle atresia by activating the p53-BAX-caspase-3 pathway.These findings reveal that WIP1 participates in regulating primordial follicle development and that inhibiting WIP1 phosphatase leads to massive primordial follicle loss via interaction with the p53-BAX-caspase-3 pathway. This might also provide valuable information for understanding decreased ovarian reserve during ovarian ageing.
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