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Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

ABSTRACT: Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

PROVIDER: PRJNA648327 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12316658.fastq.gz	Fastqsanger.gz
	SRR12316659.fastq.gz	Fastqsanger.gz
	SRR12316660.fastq.gz	Fastqsanger.gz

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Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

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Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

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An Exploratory Proteomics Study of Autoimmune Premature Ovarian Insufficiency in a Mouse Model

Project description:Premature ovarian insufficiency (POI) impairs fertility and health in reproductive-age women, with autoimmune factors contributing to 4-30% of cases[1]. To investigate immune dysregulation in POI, we developed two mouse models using pZP3 induction: regular immune (RE-POI) and enhanced immune (EN-POI) cycles. The EN-POI model exhibited stable, irreversible ovarian dysfunction, including disrupted estrous cycles, hormonal changes (elevated FSH, decreased AMH and estradiol), follicular depletion, and infertility. Immune profiling revealed increased CD4+ T cells and decreased regulatory T cells in the spleen, elevated inflammatory cytokines (e.g., interferon-γ, CCL4, CCL5) in serum, and ovarian fibrosis. Proteomics identified 198 differentially expressed proteins enriched in immune and inflammatory pathways. Network analysis highlighted six hub proteins, such as MMP9, ISG15, and IKBKE, with expressions negatively correlating with ovarian reserve markers in human POI. This study establishes a stable autoimmune POI model, elucidates T-cell imbalance with cytokine storm and fibrosis, and identifies key molecules linking immune abnormalities to ovarian failure, offering new insights for POI research.

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Project description:In order to understand how in vitro culture affects embryonic quality, we analyzed survival and global gene expression in bovine blastocysts after exposure to increased oxidative stress conditions of IVC. A pro-oxidant agents that act intra-cellularly by inhibiting GSH synthesis (0.4 mM buthionine sulfoximine [BSO]) was added from days 3 to 7, and transcriptomic analysis was then performed in resulting blastocysts. Precisely, after in vitro maturation and fertilization, bovine zygotes were culture in vitro in normal condition, then at day 3, embryos were allocated into culture in control or supplemented with BSO (0.4 mM) until day 7. At this time, blastocysts were harvested and analyzed. Our hypothesis was that BSO treatment will affect blastocyst survival and gene expression associated with low embryo quality

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