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Spatial transcriptomics reveals tanscriptional perturbations leading to uterine squamous metaplasia, atrophy, and infertility in a mouse model of RTHa

ABSTRACT: Spatial transcriptomics reveals tanscriptional perturbations leading to uterine squamous metaplasia, atrophy, and infertility in a mouse model of RTHa

PROVIDER: PRJNA1144113 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30125900_1.fastq.gz	Fastqsanger.gz
	SRR30125900_2.fastq.gz	Fastqsanger.gz
	SRR30126000_1.fastq.gz	Fastqsanger.gz
	SRR30126000_2.fastq.gz	Fastqsanger.gz
	SRR30125901_1.fastq.gz	Fastqsanger.gz

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Spatial transcriptomics reveals tanscriptional perturbations leading to uterine squamous metaplasia, atrophy, and infertility in a mouse model of RTHa

Project description:This study identifies an unknown role for KLF9 signaling in normal uterine development, which is decreased in a mouse model of resistance to thyroid hormone (RTHa), resulting in infertility through ectopic IL-33 expression produced by abnormally differentiated, KLF9-deficient endometrial cells. Utilizing a combination of genetically engineered mouse models, histopathology, spatial transcriptomics, and pharmacological inhibitors, we revealed that infertility in RTHa results from abnormal endometrial differentiation mediated by KLF9 suppression. These abnormally differentiated endometrial cells were the source of ectopic IL-33 overexpression. Increased endometrial IL-33 led to T-cell infiltration, destruction of glands, and endometrial fibrosis, which culminated in infertility. This study uncovers a link between TRa1 and KLF9 signaling for normal endometrial differentiation, reveals a mechanism for ectopic uterine IL-33 in female fertility, and provides new insights on the impact of hypothyroidism in female reproduction.

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Interleukin 27 Protects From Gastric Atrophy and Metaplasia During Chronic Autoimmune Gastritis

Project description:Background & Aims: The association between chronic inflammation and gastric carcinogenesis is well established, but it is not clear how immune cells and cytokines regulate this process. We investigated the role of interleukin 27 (IL27) in the development of gastric atrophy, hyperplasia, and metaplasia (preneoplastic lesions associated with inflammation-induced gastric cancer) in mice with autoimmune gastritis. Methods: We performed studies with TxA23 mice (control mice), which express a T-cell receptor against the H+/K+ adenosine triphosphatase α chain and develop autoimmune gastritis, and TxA23xEbi3-/- mice, which develop gastritis but do not express IL27. In some experiments, mice were given high-dose tamoxifen to induce parietal cell atrophy and spasmolytic polypeptide-expressing metaplasia (SPEM). Recombinant IL27 was administered to mice with mini osmotic pumps. Stomachs were collected and analyzed by histopathology and immunofluorescence; we used flow cytometry to measure IL27 and identify immune cells that secrete IL27 in the gastric mucosa. Single-cell RNA sequencing was performed on immune cells that infiltrated stomach tissues. Results: We identified IL27-secreting macrophages and dendritic cell in the corpus of mice with chronic gastritis (TxA23 mice). Mice deficient in IL27 developed more severe gastritis, atrophy, and SPEM than control mice. Administration of recombinant IL27 significantly reduced the severity of inflammation, atrophy, and SPEM in mice with gastritis. Single-cell RNA sequencing showed that IL27 acted almost exclusively on stomach-infiltrating CD4+ T cells to suppress expression of inflammatory genes. Conclusions: In studies of mice with autoimmune gastritis, we found that IL27 is an inhibitor of gastritis and SPEM, suppressing CD4+ T-cell–mediated inflammation in the gastric mucosa.

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