Abstract
BackgroundPremature ovarian insufficiency (POI) is characterized by abnormal ovarian function before the age of 40. POI showed that primordial follicles developed in disorder. mTOR signaling plays a vital role in the process of follicle development. It has been verified that the mTOR signaling pathway activator, MHY1485, can promote primordial follicle development in mice. We considered that MHY1485 would be a promising fertility preservation method for POI patients.MethodsThe fragmented ovarian tissues of normal woman was cultured with activator MHY1485 in vitro, and then the control and activated ovaries were transplanted into the kidney capsules of ovariectomized mice. We then used the Infinium Human Methylation EPIC BeadChip to verify the DNA methylation level of ovarian tissues, thus exploring the effectiveness of them.ResultsMHY1485 stimulated mTOR, S6K1, and rpS6 phosphorylation. Cultured with MHY1485, ovarian weights increased and endocrine function was restored. The number of growing follicles was increased. The in vitro activation process did not induce histological changes or abnormal DNA methylation occurrence.ConclusionMHY1485 for in vitro activation (IVA) is effective for ovarian rejuvenation and is a potential therapeutic treatment for POI patients.
Highlights
Premature ovarian insufficiency (POI) is a clinical syndrome in women, characterized by menstrual disturbance with an elevated follicle stimulating hormone (FSH) level and low estradiol content
Given that MHY1485 could activate the Mammalian Target of Rapamycin (mTOR) pathway in mouse ovaries and lead to the birth of offspring mice, we investigated the activation of the mTOR signaling pathway in human ovarian tissues treated with MHY1485
It is worth noticing that there is no significant difference between the 10 μM MYH1485 group and 20 μM MYH1485 group, which indicates that 10 μM may be the maximal activation concentration of MYH1485 to the mTOR pathway
Summary
Premature ovarian insufficiency (POI) is a clinical syndrome in women (age
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