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RNA-Seq Facilitates Quantitative Analysis of Wild Type and Bnc1tr/tr oocyte Transcriptomes

ABSTRACT: Primary ovarian insufficiency (POI) is a clinical syndrome of ovarian dysfunction characterized by premature exhaustion of primordial follicles. POI causes infertility, serious daily life disturbances and long-term health risks. However, the underlying mechanism remains largely unknown. We have previously identified Basonuclin1 (BNC1) mutation from a large Chinese POI pedigree and find the targeted Bnc1 mutation mouse exhibites POI. In this study, we find that BNC1 plays a key role in the dynamic balance of ovarian reserve, and maintaining lipid metabolism and redox homeostasis in oocytes during follicular development. Deficiency of BNC1 results in premature follicular activation and accelerated follicular atresia, but doesn’t affect the ovarian primordial follicle reserve. Mechanistically, BNC1 targets the NF2-YAP pathway to trigger oocyte ferroptosis. Inhibition of ferroptosis significantly rescues POI. These findings uncover a novel pathologic mechanism of POI based on BNC1 deficiency and is the first report showing ferroptosis involved in oocyte death.

ORGANISM(S): Mus musculus

PROVIDER: GSE194194 | GEO | 2022/08/31

REPOSITORIES: GEO

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RNA-Seq Facilitates Quantitative Analysis of Wild Type and Bnc1tr/tr ovary Transcriptomes

Project description:Primary ovarian insufficiency (POI) is a clinical syndrome of ovarian dysfunction characterized by premature exhaustion of primordial follicles. POI causes infertility, serious daily life disturbances and long-term health risks. However, the underlying mechanism remains largely unknown. We have previously identified Basonuclin1 (BNC1) mutation from a large Chinese POI pedigree and find the targeted Bnc1 mutation mouse exhibites POI. In this study, we find that BNC1 plays a key role in the dynamic balance of ovarian reserve, and maintaining lipid metabolism and redox homeostasis in oocytes during follicular development. Deficiency of BNC1 results in premature follicular activation and accelerated follicular atresia, but doesn’t affect the ovarian primordial follicle reserve. Mechanistically, BNC1 targets the NF2-YAP pathway to trigger oocyte ferroptosis. Inhibition of ferroptosis significantly rescues POI. These findings uncover a novel pathologic mechanism of POI based on BNC1 deficiency and is the first report showing ferroptosis involved in oocyte death.

2022-08-31 | GSE194196 | GEO

Genome-wide maps of chromatin state in Wild Type mouse ovary

2022-08-31 | GSE194195 | GEO

Differences in miRNA expression profiles of follicular fluid exosomes between Premature ovarian insufficiency and normal ovarian reserve

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Project description:The reproductive lifespan in mammals is largely determined by the abundance and quality of oocytes residing within the primoridial ovarian follicular pool. Critical oocyte-expressed genes driving ovarian function have been identified, buta role for post-translational modifications, such as SUMOylation of these key factors is not well understood. Oocyte-specific genetic ablation of the sole E2 SUMOylation enzyme, UBC9, cause female sterility. Preantral and antral stage ovarian follicles are depleted by sexual maturity, and loss of the ovarian reserve in early adulthood causes premature ovarian failure, a condition associated with infertility in women. Gene expression changes indicate atered function of multiple POI candidate genes, including the transcription factors, NOBOX and SOHLH1. Together, these studies show that SUMOylation is required in the mammalian oocyte for regulating key genetic determinants of oocyte growth and differentiation.

2019-11-15 | GSE133179 | GEO

Transcriptome analysis during VCD exposure-induced POI in mice

Project description:4-vinylcyclohexene diepoxide (VCD) is a reproductively toxic environmental pollutant that causes follicular failure leading to POIs, which can seriously affect a woman's physical health and fertility. Investigating its pathogenic mechanisms can help provide guidance for the prevention of ovarian impairment and the treatment of POI. We built a mouse model of POI by intraperitoneal injection of VCD into female C57BL/6 mice for 15 days. Then compared it with the control group at two time points, day 15 and day 30, including the comparison of phenotypic characteristics and differences in the transcriptome. We performed a comprehensive analysis of the differential genes identified and validated some key genes by RT-PCR. The results showed that sex hormone levels, follicle number and estrous cycle of VCD-induced POI mice were significantly affected at both day 15 and day 30. Regarding DEGs and enrichment results, the results obtained at day 15 were not as significant as those at day 30. Our results provide a preliminary indication that steroid hormone synthesis, DNA damage repair, and impaired oocyte mitosis play an important part in the process by which VCD affects ovarian function. Maybe it was due to impaired follicular development caused by VCD damage to the primordial follicular pool, and with the progression of time, the ovarian damage was aggravated, and it was gradually difficult to perform normal function.

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small non-coding RNA sequencing of human cumulus cells from patients with or without Diminished ovarian reserve

Project description:This group consist of human embryologists from the reproductive medical center for of the 1st affiliated hospital of Anhui Medical University. Our research is specifically focused on women ovarian reserve and the relevant female infertility. By deep sequencing, the current experiment determined the small non-coding RNA profile of cumulus cells from patients with or without diminished ovarian reserve undergoing controlled ovarian stimulation and in vitro fertilization treatment. Ovarian follicles, which are a densely-packed shell of granulosa cells that contains an immature or mature oocyte, are above all responsible for the development, maturation, and release of mature egg for fertilization. They are also responsible for synthesizing and secreting hormones that are essential for follicular development, menstrual and estrous cycle, maintenance of the reproductive tracts and their functions, development of female secondary sex characteristics, and metabolism. During folliculogenesis, ovarian granulosa cells surrounding the oocyte differentiate into mural granulosa cells, involved in gonadal steroidogenesis, and into cumulus cells, which are ovulated with the oocyte at ovulation. In the present study, we described the small non-coding RNA expression profile to characterize the ensemble of both known and novel ncRNAs expressed in cumulus cells from patients with or without Diminished ovarian reserve, by using high-throughput Solexa technology.

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Female Infertility: Primary ovarian insufficiency

Project description:<p>Premature ovarian failure, or primary ovarian insufficiency (POI) is a phenotype of diminished or absent ovarian function occurring in 1-2% of reproductive aged women. Most cases occur spontaneously. Evaluation of the gametes in women with POI is difficult and invasive. Practitioners must often rely on indirect biomarkers of ovarian function and oocyte health, making it difficult to identify patients who may benefit from therapies allowing them to achieve pregnancy utilizing their own oocytes. This study will generate exome sequences from POI patients in an effort to elucidate the causes of unexplained POI and to better understand the normal processes of ovarian aging. A better understanding of the genetics of ovarian function may lead to new non-invasive tools for managing women's reproductive health, and direct better use of existing biomarkers in diagnosis, screening and predicting clinical outcomes. </p>

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Human platelet-rich plasma promotes the primordial follicle activation through the PI3K/Akt signaling pathway

Project description:The activation of dormant primordial follicles is a promising method for rescuing the infertility of aged women and premature ovarian insufficiency (POI) patients. Accumulating evidences in both human and animal suggest that human platelet-rich plasma (hPRP) has the ability to recover ovarian function and promote follicle growth, however the underlying mechanisms remain unclear. In the current study, we revealed that hPRP promoted the activation of primordial follicles and the proliferation of granulosa cells. hPRP treatments significantly increased the levels of phosphorylated protein kinase B (Akt) and forkhead Box O3a (FOXO3a), and the number of oocytes with FOXO3a nuclear export. The hPRP-induced primordial follicle activation could be blocked by LY294002, the inhibitor of PI3K/Akt. By in vivo injection newborn mice model and in vitro culture human ovarian fragments, hPRP was further proved to be effective in the activation of primordial follicles. Taken together, our results suggest that hPRP can promote the primordial follicle activation through the PI3K/Akt pathway. Our results provide a theoretical basis for the clinical application of hPRP in aged women and POI patients.

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Inflammatory Bowel Disease Leads to Long-Term Ovarian Dysfunction via Immune-Mediated Follicular Aging

Project description:The rising global incidence of inflammatory bowel disease (IBD) is associated with reduced levels of anti-Müllerian hormone (AMH), a key biomarker for premature ovarian insufficiency (POI), highlighting reproductive risks for women of childbearing age. To investigate the connection between IBD and ovarian aging, we used a dextran sodium sulfate (DSS)-induced mouse model of IBD and assessed reproductive outcomes, including ovarian reserve, folliculogenesis, hormone profiles, and estrous cyclicity. Transcriptomic analysis of ovarian tissue showed that IBD upregulates genes associated with aging. Gene Ontology enrichment pointed to signaling pathways involved in cellular senescence, oxidative stress response, and senescence-associated secretory phenotypes. By integrating our ovarian transcriptomic data with single-cell RNA-seq datasets from young (3-month) and aged (9-month) mouse ovaries, we found significant parallels between IBD-induced transcriptional changes and natural ovarian aging. Flow cytometry confirmed elevated levels of T cells, CD8+ T cells, and macrophages in the ovaries, indicating localized immune activation. Similar systemic immune changes were observed in peripheral blood mononuclear cells, with expanded T cell and macrophage populations. TUNEL assays and qPCR further validated accelerated ovarian aging in IBD mice, showing increased granulosa cell apoptosis and upregulated aging-related markers. Notably, even after an 89-day recovery period following DSS treatment, persistent deficits in follicular counts, hormonal balance, and estrous regularity indicated irreversible ovarian dysfunction. Our findings demonstrate that IBD triggers ovarian inflammation, depletes ovarian reserve, and accelerates aging processes, leading to long-term reproductive impairment. This study elucidates the mechanistic links between IBD and POI, providing insights for therapeutic strategies to mitigate fertility risks in affected women.

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Project description:The ovarian reserve defines the female reproductive lifespan, which in humans spans decades due to robust maintenance of meiotic arrest in oocytes residing in primordial follicles. Epigenetic reprogramming, including DNA demethylation, accompanies meiotic entry, but the chromatin changes that underpin the generation and preservation of ovarian reserves are poorly defined. We report that the Polycomb Repressive Complex 1 (PRC1) establishes repressive chromatin states in perinatal mouse oocytes that directly suppress the gene expression program of meiotic prophase-I and thereby enable the transition to dictyate arrest. PRC1 dysfuction causes depletion of the ovarian reserve and leads to premature ovarian failure. Our study demonstrates a fundamental role for PRC1-mediated gene silencing in female reproductive lifespan, and reveals a critical window of epigenetic programming required to establish ovarian reserve.

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