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Single cell RNA sequencing analysis of Mig-6 mutant mouse reveals progesterone susceptibility genes for uterine receptivity

ABSTRACT: Single cell RNA sequencing analysis of Mig-6 mutant mouse reveals progesterone susceptibility genes for uterine receptivity

PROVIDER: PRJNA1227122 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32456641_1.fastq.gz	Fastqsanger.gz
	SRR32456641_2.fastq.gz	Fastqsanger.gz
	SRR32456642_1.fastq.gz	Fastqsanger.gz
	SRR32456642_2.fastq.gz	Fastqsanger.gz

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Single cell RNA sequencing analysis of Mig-6 mutant mouse reveals progesterone susceptibility genes for uterine receptivity

Project description:The majority of pregnancy losses result from implantation failure. Successful embryo implantation involves a delicate interaction between the receptive uterus and an implantation-competent blastocyst. Understanding the mechanisms regulating the endometrial receptivity during preimplantation are essential for improving pregnancy outcomes. Mitogen-inducible gene 6 (MIG-6) is a key mediator of progesterone signaling in the endometrium.MIG-6 loss results in implantation failure due to non-receptive endometrium. We applied single cell RNA sequencing to determine the composition of different cell types and functions within non-receptive endometrium from uterine specific Mig-6 knock-out (Pgrcre/+Mig-6f/f; Mig-6d/d) mice. Mig-6d/d mice revealed altered gene expression in the epithelial and stromal cells. We identified key gene expression changes in the non-receptive endometrium of Mig-6d/d mice, providing valuable insights into the role of progesterone signaling in implantation.

2025-03-21 | GSE290275 | GEO

Uterine glands impact uterine receptivity, luminal fluid homeostasis and blastocyst implantation

Project description:Uterine glands are essential for pregnancy in mice and likely humans, because they secrete or transport bioactive substances that regulate uterine receptivity for blastocyst implantation. In mice, the uterus becomes receptive to blastocyst implantation on day 4, but is refractory by day 5. Here, blastocysts could be recovered from progesterone-induced uterine gland (PUGKO) but not wildtype (WT) mice on day 5 post-mating. Anti-adhesive Muc1 protein and microvilli were present on the luminal epithelium of PUGKO but not WT uteri. A number of known uterine receptivity genes and gland-specific genes were altered in the PUGKO uterus. Next, the uterus and uterine luminal fluid (ULF) were obtained from WT and PUGKO mice on day 3, 4 and 5. Transcriptome analysis revealed that 580 genes were decreased in the PUGKO uterus, however ULF secrotome analysis revealed that many proteins and several amino acids were increased in the PUGKO ULF. Of note, many proteins encoded by many gland-specific genes were not identified in the ULF of WT mice. These results support the ideas that uterine glands secrete factors that regulate ULF homeostasis and interact with other cell types in the uterus to influence uterine receptivity and blastocyst implantation for the establishment of pregnancy.

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Pathophysiological role of MIG-6 and ERBB2 in progesterone resistance and endometriosis-related infertility.

Project description:MIG-6 loss caused progesterone resistance through ERBB2 overexpression in non-receptive endometrium of endometriosis-related infertility. We used microarrays to understand the molecular mechanisms of progesterone resistance in infertility

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Progesterone receptor in uterine glands is required for pregnancy establishment in mice

Project description:By utilizing Prss29-Cre, Pgr was conditionally deleted to identify the definitive roles of progesterone signaling in the uterine glands during pregnancy. This study provides new insights, demonstrating that PGR-P4 signaling in the glandular epithelium is required for uterine receptivity by regulating LIF on gestation day 4. Furthermore, we have shown that PGR signaling in glands is dispensable post-implantation.

2025-03-26 | GSE292591 | GEO

The impact of progesterone levels and timing of progesterone exposure on human endometrial receptivity

Project description:Different progesterone levels and timing of exposure results in different endometrial gene expression and implantation potential. Sufficient progesterone level is important to induce endometrial receptivity and endometrial expressed the most receptive stage after exposure to progesterone for 7 days based on decidualisation marker expression.

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Endometrial Cancer Susceptibility Gene CTCF is Essential for Progesterone Dependent Uterine Maturation

Project description:Endometrial Cancer Susceptibility Gene CTCF is Essential for Progesterone Dependent Uterine Maturation

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METTL3-dependent m6A methylation facilitates uterine receptivity and female fertility via balancing estrogen and progesterone signaling

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Endometrial Cancer Susceptibility Gene CTCF is Essential for Progesterone Dependent Uterine Maturation

Project description:Receptors for estrogen and progesterone frequently interact, via Cohesin/CTCF loop extrusion, at enhancers distal from regulated genes; CTCF is decreased or mutated in >20% of human endometrial tumors, indicating its importance in uterine homeostasis. To better understand how CTCF-mediated enhancer-gene interactions impact endometrial development and function, the Ctcf gene was selectively deleted in female reproductive tissues of mice. Prepubertal Ctcfd/d uterine tissue exhibited normal morphology, with a significant reduction in the number of uterine glands compared to those without Ctcf deletion (Ctcff/f mice). Post-pubertal Ctcfd/d uteri were hypoplastic with significant reduction in both the size of the endometrial stroma and number of glands. Transcriptional profiling revealed increased expression of stem cell molecules Lif, EOMES and Lgr5, and enhanced inflammation pathways following Ctcf deletion. Analysis of the response of the uterus to steroid hormone stimulation showed that the response of the uterus to estrogen was not impacted, but that CTCF deletion affects a subset of progesterone responsive genes. This finding indicates 1) mediators of P signaling remain functional following Ctcf deletion and 2) certain P regulated genes are sensitive to Ctcf deletion, suggesting they depend on gene-enhancer interactions that require CTCF. The P responsive genes altered by CTCF ablation included Ihh, Fst and Errfi1, as well as other genes involved in the regulation of critical processes including hormone response, transcription, and inhibition of tumor generation. Overall, our findings reveal that uterine Ctcf plays a key role in P dependent expression of uterine genes underlying optimal post pubertal uterine development.

2024-08-08 | GSE227517 | GEO

Enhancing Uterine Receptivity for Embryo Implantation through Controlled Collagenase Intervention

Project description:Ineffective endometrial matrix remodeling, a key factor in infertility, impedes embryo implantation in the uterine wall. Our study reveals the cellular and molecular impact of human collagenase-1 administration in mouse uteri, demonstrating enhanced embryo implantation rates. Collagenase-1 promotes remodeling of the endometrial extracellular matrix (ECM), degrading collagen fibers and proteoglycans. This process releases matrix-bound bioactive factors, (e.g. VEGF, decorin), facilitating vascular permeability and angiogenesis. Collagenase-1 elevates embryo implantation regulators, including NK cell infiltration and the key cytokine LIF. Remarkably, uterine tissue maintains structural integrity despite reduced endometrial collagen fiber tension. In-utero collagenase-1 application rescues implantation in the heat stress and embryo transfer models, known for low implantation rates. Importantly, ex-vivo exposure of human uterine tissue to collagenase-1 induces collagen de-tensioning and VEGF release, mirroring remodeling observed in mice. Our research highlights collagenase potential to induce and orchestrate cellular and molecular processes enhancing uterine receptivity for effective embryo implantation. This innovative approach underscores ECM remodeling mechanisms critical for embryo implantation

2024-08-13 | PXD054389 | Pride

Progesterone increases metabolism via the pentose phosphate pathway in bovine uterine epithelial cells

Project description:During early pregnancy, glucose is essential for the uterine epithelium and the developing embryo. In cows, studies have shown that progesterone increases the secretion of glucose into the uterine lumen. Nevertheless, how progesterone affects glucose metabolism in the uterine epithelium has been sparsely investigated. Therefore, our objective was to investigate how progesterone influences glucose metabolism in immortalized bovine uterine epithelial (BUTE) cells. Progesterone treatment (10 μM) increased glucose consumption. To gain a more global picture of the effects of progesterone, RNAseq was performed after BUTE cells were treated with vehicle (DMSO) or 10 μM for 24 hours. KEGG analysis indicated that progesterone altered genes associated with metabolic pathways and glutathione metabolism. Manually examining genes unique to specific glucose metabolic pathways identified an increase in the rate-limiting enzyme in the pentose phosphate pathway—glucose-6-phosphate dehydrogenase. Functionally, a major product of the pentose phosphate pathway is NADPH, and progesterone treatment increased NADPH concentrations in BUTE cells. In cows, immunohistochemistry confirmed that glucose-6-phosphate dehydrogenase levels were higher in the uterine epithelium in the luteal phase when progesterone concentrations are high. In conclusion, progesterone increased glucose-6-phosphate dehydrogenase expression and metabolism via the pentose phosphate pathway in the bovine uterine epithelium. This metabolism could provide substrates for cell proliferation, molecules to be secreted into the uterine lumen that supports embryonic development, or maintain reduction/oxidation balance in the uterine epithelium.

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