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• W2335800888 abstract "Survival rates from many childhood cancers have increased dramatically over the past 50 years. Many of these survivors were treated with lifesaving medications that had the unfortunate adverse effect of reducing their fertility or causing sterility. There are only two options currently for reproductive aged women to preserve fertility; egg retrieval or ovarian tissue freezing. Lupron remains the one pharmacologic treatment, that is offered to young women undergoing chemotherapy with hope of placing ovaries in a quiescent state prior to undergoing treatment, however GnRH agonist treatment with chemotherapy does not prevent or ameliorate ovarian damage and follicle loss in vitro (1). Female fertility depends on a delicate balance of hormones and their receptors, signaling molecules, and transcription factors which regulate ovarian function. Many of these factors are not known, or have only been studied in animal models. Once particular gene, FOX03a, which is in the family of forehead box transcription factors, has been shown in the mouse model to be an important regulator of ovarian folliculogenesis in both theca and luteal cells (2). The transcription factor Foxo3a impacts apoptosis, metabolism, and cell proliferation/differentiation, and is critical in ovarian folliculogenesis. Mice overexpressing Foxo3a in the ovary are infertile due to lack of follicular development, while Foxo3a-/-mice display infertility resulting from global follicular activation. By understanding the role of FOX03a, we may better understand how gonadal toxic drugs in children and adolescents may lead to premature ovarian failure and infertility. 5-week-old C57/B6 female mice were injected daily with 2-deoxyglucose (2-DG), a glucose-deprivation mimetic, at increasing concentrations (100mg/kg, 300mg/kg, 600mg/kg or PBS). The RNA analysis was completed using Real Time PCR to show expression level of Fox03A. The contralateral ovary was formalin-fixed and sectioned, and follicles were counted and classified. Our cell culture data show that Foxo3a mRNA and protein expression is induced by both essential amino acid and glucose deprivation. We hypothesized that nutrient deprivation in mice would similarly upregulate Foxo3a expression, and potentially block follicular development. 5-week-old C57/B6 female mice were injected daily with 2-deoxyglucose (2-DG), a glucose-deprivation mimetic, at increasing concentrations (100mg/kg, 300mg/kg, 600mg/kg or PBS). After two weeks, one ovary was used for RNA analysis, which showed that 100mg/kg 2-DG caused a 4-fold increase in Foxo3a mRNA. Mice treated with 100mg/kg 2-DG had a 58% decrease in percentage of early-stage primary follicles, while treatment with 600mg/kg 2-DG resulted in a 32% decrease in these follicles. Our data demonstrate that nutrient deprivation induces Foxo3a in a mouse model, and that this induction results in a decrease of early-stage activated follicles. Most importantly, it has been shown to be imperative in the periodic activation and maturation of primordial follicles. When ovarian follicles make this transition from prenatal to antral follicles, it depletes the number of follicles a woman has and therefore influences the duration of her fertility. Our current study now seeks to determine if FOX 03A is present in human ovarian tissue and if so, if it responds to these deprivation conditions similarly to the mouse model. This project will lead to better understanding of the maturation of these primordial follicles." @default.
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• W2335800888 date "2016-04-01" @default.
• W2335800888 modified "2023-09-26" @default.
• W2335800888 title "Induction of Fox03a by Nutrient Deprivation Regulates Folliculogenesis" @default.
• W2335800888 doi "https://doi.org/10.1016/j.jpag.2016.01.102" @default.
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