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Molecular medicine reports

Molecular medicine reports

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Role of cellular prion protein in mouse granulosa cells and its effects on ovarian function in knockout mice

Published:1 October 2025 DOI: 10.3892/mmr.2025.13630 PMID: 40709399
Qinyue Cao,?Hehua Wang,?Jingjing Hu,?Yan Wang,?Tong Dai,?Fen Liu,?Xia Yang,?Qinyu Yang,?Chunhua Tu

Abstract

Cellular prion protein (PrPc) regulates ovarian reserve maintenance through anti?Müllerian hormone (AMH)?dependent mechanisms. The present study explored the role of PrPc in the ovarian function of mice using complementary in vitro and in vivo models. First, prion protein gene (PRNP) knockdown or overexpression was carried out in mouse ovarian granulosa cells. In vitro analyses conducted using flow cytometry and ELISA revealed that the depletion of PrPc specifically hindered the secretion of AMH compared with control groups, while the levels of progesterone (P4) and estradiol (E2) remained unchanged across all experimental groups. Importantly, the reduction in AMH levels was reversed upon re?expression of PrPc. Additionally, neither the distribution of the cell cycle nor the rates of apoptosis were affected by the manipulation of PrPc. Subsequently, a comparative analysis of mice with PRNP knockout (KO) vs. wild?type mice was performed. However, PrPc depletion did not alter the production of progesterone or estradiol. Whilst the ovarian histology remained intact in KO mice, an elevation in follicle?stimulating hormone levels was observed, thereby suggesting a potential involvement of compensatory neuroendocrine regulation. These findings revealed that PrPc may be a novel modulator for maintaining the ovarian reserve which depends on AMH. The present study redefined the molecular landscape of ovarian reserve depletion by identifying the dysfunction of the PrPc?AMH axis as a possible reason for diminished ovarian reserve syndromes.

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