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

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

PROVIDER: PRJNA858272 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20139751_1.fastq.gz	Fastqsanger.gz
	SRR20139751_2.fastq.gz	Fastqsanger.gz
	SRR20139752_1.fastq.gz	Fastqsanger.gz
	SRR20139752_2.fastq.gz	Fastqsanger.gz
	SRR20139753_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

Project description:To investigate the effect of Mettl3 in the uterus, we generated mice with conditional ablation of Mettl3 in progesterone receptor (PR)–positive cells (PgrCre Mettl3 fl/fl). And the uterus of Mettl3 cKO and control mice on GD4 were obtained for RNA-seq analysis.

2023-09-07 | GSE208096 | 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.

2020-03-12 | GSE146777 | 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.

2016-11-22 | GSE90101 | GEO

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

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

| PRJNA611948 | ENA

Decreased epithelial Progesterone Receptor A at the window of receptivity is required for preparation of the endometrium for embryo attachment

Project description:The progesterone receptor A (PGRA) isoform is the dominantly expressed isoform within the mouse uterus and is indispensable for uterine function and fertility in the murine reproductive tract. During early pregnancy, the PGRA isoform is spatiotemporally expressed in the uterine epithelium. At days 2-3 of pregnancy, PGRA is upregulated within the epithelium and then decreases before day 4, the day of embryo implantation. This decrease of PGRA has been recognized as a marker to initiate the time in which the uterus is receptive to the embryo, yet this has never been functionally tested. We hypothesized the decrease of PGRA at the window of receptivity is required for successful embryo implantation. In order to test this hypothesis, we generated a PGRA conditional expression allele initiated by Cre recombinase present in the uterine epithelial compartment. The PGRA expressing mice exhibited infertility with the inability to undergo embryo implantation or decidualization. RNA microarray and ChIP-Seq analyses were utilized to identify the differentially regulated pathways controlled by PGRA at the time of implantation.

2019-08-29 | GSE86303 | GEO

Concentrations of progesterone prior to luteolysis modulates the uterine luminal transcriptome in the subsequent cycle in cattle

Project description:Sex-steroids concentrations throughout the estrous cycle modulate endometrial function and fertility in cattle. The objective of this study was to compare the post-estrus endometrial transcriptome of cows that were exposed to contrasting pre-estrus concentrations of progesterone before they displayed estrus and ovulated spontaneously. We hypothesized that greater pre-estrus concentration of progesterone alters post-estrus endometrial function even after the display of estrus and spontaneous ovulation.

2022-04-13 | GSE200361 | GEO

Progesterone responsive uterine transcriptome in rat

Project description:We have previously shown that Brown Norway (BN) rats are progesterone resistant. Thus this experiment was designed to compare the transcriptomes in uterus that are altered by progesterone challenge between this strain of rat with Holtzman Sprague Dawley (HSD) rats

2016-05-04 | GSE68542 | GEO

A luteal phase deficiency model in normal women: structural and functional responses to varying concentrations of progesterone

Project description:Progesterone (P) action is essential for embryo implantation, but the P concentration required for normal receptivity remains unclear. We use an in vivo model in normal women that abolishes detectable endogenous P production, allowing experimental provision of P. Endometrial samples on the 10th day of varying doses of P exposure are compared structurally and functionally with each other and with mid-secretory endometrium of natural cycles, using histological and microarray analysis. At 2.5mg/day of P, a delayed appearance of morphological features is seen. Higher sub-physiological levels of P result in normal morphology, but aberrant gene expression. These studies prove that low P levels can result in histological delay, consistent with clinical expectations. However, P levels required for consistent histological delay are lower than those seen in all ovulatory women. These studies also demonstrate that gene expression abnormalities can occur at higher sub-physiological P concentrations, without a change in morphology, a functional-morphological disassociation. The expression of some endometrial receptivity associated genes is multiphasic, with peak expression between the lowest and highest doses, suggesting sustained supraphysiological doses seen in fertility treatment cycles may not be optimal. These findings provide a scientific underpinning to previous studies that questioned the value of endometrial morphology as a marker for receptive endometrium and suggest potential new strategies for understanding endometrial P action. Total RNA obtained endometrium of women treated with progesterone at different doses (2.5 mg (n=4); 5 mg (n=4); 10mg (n=5_); 40 mg (n=5); Control no drug (n=9))

2014-04-23 | E-GEOD-56980 | biostudies-arrayexpress

The autophagy protein, FIP200 (RB1CC1) mediates progesterone responses governing uterine receptivity and decidualization†.

Project description:Successful establishment of pregnancy depends on steroid hormone-driven cellular changes in the uterus during the peri-implantation period. To become receptive to embryo implantation, uterine endometrial stromal cells (ESCs) must transdifferentiate into decidual cells that secrete factors necessary for embryo survival and trophoblast invasion. Autophagy is a key homeostatic process vital for cellular homeostasis. Although the uterus undergoes major cellular changes during early pregnancy, the precise role of autophagy in uterine function is unknown. Here, we report that conditional knockout of the autophagy protein FIP200 in the reproductive tract of female mice results in reduced fecundity due to an implantation defect. In the absence of FIP200, aberrant progesterone signaling results in sustained uterine epithelial proliferation and failure of stromal cells to decidualize. Additionally, loss of FIP200 impairs decidualization of human ESCs. We conclude that the autophagy protein FIP200 plays a crucial role in uterine receptivity, decidualization, and fertility. These data establish autophagy as a major cellular pathway required for uterine receptivity and decidualization in both mice and human ESCs.

| S-EPMC7124967 | biostudies-literature

Podocalyxin governs the barrier function of human endometrial epithelium and critically regulates receptivity for embryo implantation

Project description:Embryo implantation is a key step in establishing pregnancy and a major limiting factor in IVF. Implantation requires the endometrium, the inner lining of the uterus, to transform from a non-receptive to a receptive state, to allow embryos to attach to the surface and enter into the tissue. However, the fundamental mechanisms governing receptivity are not well understood. Here we show that transmembrane protein podocalyxin is a major and clinically significant factor regulating human endometrial receptivity. Podocalyxin is expressed in all endometrial epithelial cells in the non-receptive state but is selectively down-regulated in the luminal epithelium at receptivity. We present evidence that podocalyxin critically governs the barrier function of the endometrial epithelium, likely as an intrinsic protective mechanism, rendering it non-receptive to an embryo. In addition, podocalyxin suppresses genes promoting receptivity (eg LIF, CSF1) but stimulates those inhibiting implantation (eg WNT7A, LEFTY2). Down-regulation of podocalyxin in the luminal epithelium, likely mediated by progesterone, selectively converts the endometrial surface to a more adhesive state that facilitates embryo attachment and penetration. Furthermore, inadequate down-regulation of podocalyxin in the endometrial luminal epithelium is associated with poorer implantation rates in IVF. We thus propose that podocalyxin promotes the barrier function of human endometrial epithelial cells and critically regulates receptivity for embryo implantation.

2021-04-01 | GSE148274 | GEO

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