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

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

PROVIDER: PRJNA1222861 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32323637_1.fastq.gz	Fastqsanger.gz
	SRR32323637_2.fastq.gz	Fastqsanger.gz
	SRR32323638_1.fastq.gz	Fastqsanger.gz
	SRR32323638_2.fastq.gz	Fastqsanger.gz
	SRR32323639_1.fastq.gz	Fastqsanger.gz

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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.

2025-02-17 | GSE289404 | GEO

Telomere dysfunction instigates inflammation in inflammatory bowel disease

Project description:Telomere dysfunction instigates inflammation in inflammatory bowel disease

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Homozygous IL37 mutation leads to infantile inflammatory bowel disease

Project description:Homozygous IL37 mutation leads to infantile inflammatory bowel disease

| PRJNA635708 | ENA

Homozygous IL37 mutation leads to infantile inflammatory bowel disease

Project description:Homozygous IL37 mutation leads to infantile inflammatory bowel disease

| PRJNA635709 | ENA

Telomere dysfunction instigates inflammation in inflammatory bowel disease

Project description:Abstract: Inflammatory bowel disease (IBD) is a chronic inflammatory condition driven by diverse genetic and nongenetic programs that converge to disrupt immune homeostasis in the intestine. We have reported that, in murine intestinal epithelium with telomere dysfunction, DNA damage-induced activation of ataxia-telangiectasia mutated (ATM) results in ATM-mediated phosphorylation and activation of the YAP1 transcriptional coactivator, which in turn up-regulates pro-IL-18, a pivotal immune regulator in IBD pathogenesis. Moreover, individuals with germline defects in telomere maintenance genes experience increased occurrence of intestinal inflammation and show activation of the ATM/YAP1/pro-IL-18 pathway in the intestinal epithelium. Here, we sought to determine the relevance of the ATM/YAP1/pro-IL-18 pathway as a potential driver of IBD, particularly older-onset IBD. Analysis of intestinal biopsy specimens and organoids from older-onset IBD patients documented the presence of telomere dysfunction and activation of the ATM/YAP1/ precursor of interleukin 18 (pro-IL-18) pathway in the intestinal epithelium. Employing intestinal organoids from healthy individuals, we demonstrated that experimental induction of telomere dysfunction activates this inflammatory pathway.

2021-10-30 | GSE182424 | GEO

Sub-lethal stimulation of ferroptosis leads to trophoblast dysfunction

Project description:Sub-lethal stimulation of ferroptosis leads to trophoblast dysfunction

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Haploinsufficiency of the mouse Tshz3 gene leads to kidney dysfunction

Project description:Haploinsufficiency of the mouse Tshz3 gene leads to kidney dysfunction

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Pneumosepsis survival in the setting of obesity leads to persistent steatohepatitis and metabolic dysfunction.

Project description:Pneumosepsis survival in the setting of obesity leads to persistent steatohepatitis and metabolic dysfunction.

2023-05-02 | GSE231504 | GEO

proteomic investigation of ovarian follicular fluid

Project description:To investigate the relationship between differentially expressed proteins in human ovarian follicular fluid representing oocyte maturation and quality.

2021-07-26 | PXD027577 |

Drosophila CNS mitochondrial DNA dysfunction microarray

Project description:Mitochondrial DNA (mtDNA) encodes essential components of the respiratory chain and loss of mtDNA leads to mitochondrial dysfunction and neurodegeneration. Mitochondrial transcription factor A (TFAM) is an essential component of mtDNA replication and a regulator of mitochondrial copy number in cells. Studies have shown that TFAM knockdown leads to mitochondrial dysfunction and respiratory chain deficiencies. Using gene expression analysis, we aimed to investigate the effects of mtDNA dysfunction in the CNS at the molecular level. We used microarray analysis to investigate gene expression in cases of mitochondrial dysfunction in the CNS. RNA was purified from the late third instar larval CNS from control larvae, or larvae over-expressing mitochondrial transcription factor A (TFAM) in post-mitotic neurons using the neuron specific driver nsyb-Gal4. Three replicates are included for each condition.

2013-12-20 | E-GEOD-53509 | biostudies-arrayexpress

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