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Genome-wide identification of transcriptional targets for H4K12la during uterine stromal cells decidualization in mice

ABSTRACT: Genome-wide identification of transcriptional targets for H4K12la during uterine stromal cells decidualization in mice

PROVIDER: PRJNA1011345 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25845678_1.fastq.gz	Fastqsanger.gz
	SRR25845678_2.fastq.gz	Fastqsanger.gz
	SRR25845679_1.fastq.gz	Fastqsanger.gz
	SRR25845679_2.fastq.gz	Fastqsanger.gz
	SRR25845680_1.fastq.gz	Fastqsanger.gz

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Endometrial gland impacts on stromal cell decidualization

Project description:Uterine glands and, by inference, their secretions impact uterine receptivity, blastocyst implantation, stromal cell decidualization, and placental development. Changes in gland function across the menstrual cycle are impacted by steroid hormones, estrogen and progesterone, as well as stroma-derived factors. Using an endometrial epithelial organoid (EEO) system, transcriptome and proteome analyses identified distinct responses of the EEO to steroid hormones and prostaglandin E2 (PGE2). Notably, steroid hormones and PGE2 modulated the basolateral secretion of EEO proteins, where cystatin C (CST3) was significantly increased by progesterone and PGE2. CST3 treatment of decidualizing stromal cells significantly decreased the decidualization markers PRL and IGFBP1. The attenuation of stromal cell decidualization via CST3 suggests a role for uterine gland-derived proteins in controlling the extent of decidualization. These findings provide evidence that uterine gland-derived factors directly impact stromal cell decidualization, which has strong implications for better understanding pregnancy establishment and female fertility in humans.

2023-10-11 | PXD034357 | Pride

Genome-wide identification of transcriptional targets for H4K12la during uterine stromal cells decidualization in mice

Project description:To explore the potential mechanism responsible for the role of H4K12la during decidualization, we performed Cleavage Under Targets & Tagmentation (CUT&Tag) analysis using in vitro decidualization model to identify candidate genes regulated by H4K12la.

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Endometrial gland impacts on stromal cell decidualization

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Uterine glands synchronize embryo-endometrial interactions and coordinate on-time embryo implantation and stromal cell decidualization for pregnancy success

Project description:By employing FOXA2-deficient mouse models coupled with LIF repletion, we reveal definitive roles of uterine glands in pregnancy establishment.These studies provide original evidence that uterine glands synchronize embryo-endometrial interactions, coordinate on-time embryo implantation, and impact stromal cell decidualization, thereby ensuring embryo viability, placental growth, and pregnancy success.

2018-04-13 | GSE113065 | GEO

The effect of obesity on uterine receptivity is mediated by endometrial extracellular vesicles that control human endometrial stromal cell decidualization and trophoblast invasion

Project description:The objectives of the present study were to determine whether obesity impacts human decidualization and the endometrial control of trophoblast invasion (both of which are required for embryo implantation) and evaluate the potential involvement of endometrial extracellular vesicles (EVs) in the regulation of these physiological processes. Using primary human cell cultures, we first demonstrated that obesity is associated with significantly lower in vitro decidualization of endometrial stromal cells (ESCs). We then showed that the trophoblastic cell line’s invasive ability was greater in the presence of conditioned media from cultures of ESCs from obese women. Using mass-spectrometry-based quantitative proteomics, we found that EVs isolated from uterine supernatants of biopsies from obese women (vs. nonobese women) presented a molecular signature focused on cell remodeling and angiogenesis. Lastly, the results of functional assays indicated that supplementation of the culture medium with EVs from nonobese women can rescue (at least in part) the defect in in vitro decidualization described in ESCs from obese women. Lastly, the addition of endometrial EVs from obese women (vs. nonobese women) was associated with significantly greater invasive activity by HTR-8/SVneo cells. In conclusion, our results provided new insights into the endometrial EVs’ pivotal role in the poor uterine receptivity observed in obese women.

2023-10-09 | PXD039568 | Pride

Uterine-specific SIRT1 deficiency confers premature uterine aging and impairs invasion and spacing of blastocyst and stromal cell decidualization in mice.

Project description:We demonstrate that Sirtuin 1 (SIRT1) is an indispensable age-related regulator of invasion and spacing of blastocysts, as well as decidualization of stromal cells. Here, we report the sequencing of the uterine transcriptome of control and conditional knock-out of the Sirtuin 1 (SIRT1) at day 3.5 of murine pregnancy.

2022-09-14 | GSE186065 | GEO

The coregulator, repressor of Estrogen Receptor Activity (REA), is a crucial regulator of the timing and magnitude of uterine decidualization.

2013-04-04 | GSE42376 | GEO

The coregulator, repressor of Estrogen Receptor Activity (REA), is a crucial regulator of the timing and magnitude of uterine decidualization.

Project description:Our findings establish a key role for the coregulator, Repressor of Estrogen receptor Activity (REA), in controlling the timing and magnitude of decidualization in human endometrial stromal cells in vitro and in the mouse uterus in vivo, and suggest that REA functions to synchronize uterine differentiation with concurrent embryo development, which is essential for optimal implantation and fertility. The findings highlight that REA physiologically restrains endometrial stromal cell decidualization, controlling the timing and magnitude of decidualization to enable proper synchronization of uterine differentiation with concurrent embryo development that is essential for implantation and optimal fertility. Human endometrial stromal cells (hESCs) were isolated from biopsies taken from the early proliferative stage endometrium of regularly cycling women on no hormonal medications. Cells were cultured in DMEM/F-12 mediumcontaining 5% charcoal stripped fetal bovine serum. To induce in vitro decidualization, hESCs were treated with a hormone cocktail containing 10 nM estradiol (E2), 1 Î¼M progesterone (P4) and 0.5 uM 8-bromo-cAMP for up to 10 days, and media were changed every 48 h. For siRNA experiments, hESCs were transfected with REA siRNA or GL3 luciferase control siRNA following the Silent-Fect kit protocol. After 48 h of transfection, hESCs were exposed to the hormone cocktail for 24 hours or 96 hours of differentiation. key words; siRNA knock-down, hormone cocktail treatment

2013-04-04 | E-GEOD-42376 | biostudies-arrayexpress

Transcriptomic profiling of canine decidualization and effects evoked by antigestagens on decidualized canine uterine stromal cells

Project description:Maternal-stroma derived decidual cells are the single population in the canine placenta expressing the nuclear progesterone (P4) receptor (PGR), rendering them crucial for the maintenance of canine pregnancy. Indeed, decreased circulating P4 levels or blockage of PGR function with antigestagens (e.g., aglepristone), culminates in the termination of canine pregnancy. As an in vitro model for canine decidualization, dog uterine stromal (DUS; Graubner et al., 2017) cells can be decidualized in vitro with cAMP. The antigestagens aglepristone and mifepristone ablate the expression of decidualization markers in DUS cells (e.g., PGR, PRLR, IGF1 or PTGES). In order to study the mechanisms involved in feto-maternal communication during pregnancy and induction of parturition, the goal of the present work was to assess transcriptional changes mediated by decidualization and antigestagens-induced effects in decidualized DUS cells. Decidualization led to the upregulation of 1841 differentially expressed genes (DEGs, P < 0.01, FDR < 0.01) involved in cellular proliferation and adhesion, mesenchymal-epithelial transition, extracellular matrix organization, and vaso- and immunomodulation. The 1475 DEGs downregulated after decidualization were mostly associated with apoptosis and cell migration. In decidualized DUS cells, aglepristone modulated 1400 DEGs and mifepristone 1558 DEGs. Interestingly, only around half of the identified DEGs were modulated uniquely by one of the antigestagens. In both situations, however, PGR-blockage was associated with an inversion of decidualization-induced effects. Comparison between antigestagens-mediated effects and transcriptional changes in the canine placenta at term allowed the identification of 191 DEGs associated with cell proliferation and adhesion, vascularization and immune activity. These findings emphasize the importance of P4/PGR signaling for decidual cells function.

2022-12-28 | GSE213788 | GEO

Erbb2 establishes the timing of progesterone priming required for uterine receptivity

Project description:This project investigates the role of Erbb2 in regulating uterine stromal progesterone responsiveness during the peri-implantation period in mice. Using bulk RNA sequencing of stromal tissues collected on day 4 of pregnancy, we examined transcriptional alterations caused by uterine Erbb2 deletion. The data provide insight into how Erbb2 enables timely progesterone receptor activation, promotes stromal preparedness, and ensures normal implantation and decidualization. These findings contribute to understanding the molecular mechanisms governing uterine receptivity.

2025-11-17 | GSE310168 | GEO

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