Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA288706 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene expression profiling of mouse uterine epithelial cells isolated on morning of day 4 of pregnancy
| PRJNA188528 | ENA
Project description:Gene expression profiling of uterine epithelial cells isolated from Msx1Msx2 floxed and Msx1Msx2 ablated mice on day 4 of pregnancy
| PRJNA154637 | ENA
Project description:Gene expression profiling of uterine stromal cells isolated from Hand2 floxed and Hand2 ablated mice on day 4 of pregnancy
| PRJNA135811 | ENA
Project description:Gene expression profiling of uterine stromal cells isolated from Msx1Msx2 floxed and Msx1Msx2 ablated mice on day 4 of pregnancy
| PRJNA154603 | ENA
Project description:Embryo implantation into a receptive endometrium is tightly regulated by a variety of maternal factors, including cytokines, growth factors and transcription factors. Previous studies identified the leukaemia inhibitory factor (LIF), produced in uterine glands, as an essential factor for implantation. It was shown that LIF acts via its cell surface receptor to activate the transcription factor STAT3 in the uterine epithelial cells. However, the mechanisms via which STAT3 promotes uterine receptivity remain unknown. To address the molecular pathways regulated by STAT3 in the uterus, we created mice in which Stat3 gene is conditionally inactivated in uterine epithelium. These mutant mice are infertile due to implantation failure and exhibit a lack of embryo attachment to the luminal epithelium. Gene expression profiling of the epithelial tissue impaired in STAT3 activation revealed dysregulated expression of specific components of junctional complexes, including E-cadherin, M-NM-2-catenin, and claudins, which critically regulate epithelial cell polarity and embryo attachment. Additionally, mice lacking functional epithelial STAT3 showed markedly reduced stromal proliferation and differentiation, indicating that this transcription factor controls stromal function via a paracrine mechanism. The stromal defect arose from a drastic reduction in the production of several members of the epidermal growth factor (EGF) family in luminal epithelium of mutant uteri and consequent lack of activation of EGF receptor signaling and mitotic activity in the stromal cells. Collectively, our results uncovered intricate signaling networks operating downstream of STAT3 in uterine epithelium that regulate epithelial cell polarity, and stromal proliferation and differentiation, which are critical determinants of successful implantation. To identify the downstream targets of STAT3 in mouse uterine epithelial cells during pregnancy, we performed gene expression profling of mouse uterine epithelial cells on day 4 of pregnancy between Stat3 flox control and SW d/d mice. This led to the identification of several junctional molecules (Claudins and Catenins) that are negatively regulated by STAT3 at the time of implantation. Mouse uteirne epithelial cells were isolated from control and knockout mice on the morning of day 4 of pregnancy. (n=3 for each sample), pooled total RNA from these cells was then hybridized to high density affymetrix microarrays according to the Affymetrix protocol (Mouse Genome 430A 2.0 Array) .
2013-07-01 | E-GEOD-44087 | biostudies-arrayexpress
Project description:This study investigates cadmium-induced proteomic alterations in gestational day 8 decidua using a uterine-localized exposure mouse model. Female ICR mice (7-8 weeks) received daily vaginal CdCl₂ (0.01 mg/mL, 100 μL) under isoflurane anesthesia (n=3 biological replicates). Tissues were snap-frozen in liquid nitrogen post-GD8 collection. Ultra Deep quantitative proteomics with diaPASEF acquisition (timsTOF Pro2, Wuhan Maiwei) revealed differential protein expression profiles associated with Cd exposure during early pregnancy.
2025-03-19 | PXD062021 |
Project description:Uterine receptivity (the window of implantation) is essential for successful implantation. The concept of uterine receptivity was first discovered 50 years ago by Psychoyos. In mice, uterine receptivity begins with the secretion of LIF from uterine glands stimulated by estrogen on the morning of day 4 pregnancies. However, some implantation failure is due to the lack of responses to the estrogen secretion. The current study reveals that uterine glands undergo a differentiation process with increases in more branches during the preimplantation period. The single cell RNA profiling of glandular cells identifies that LIF is expressed exclusively in a Prss29+ subgroup of glands in response to estrogen secretion on day 4 of pregnancy. Previous studies have shown that Foxa2 deficiency in uterine glands results in implantation failure due to lack of LIF production. Interestingly, Foxa2-deficient glands fail to develop branches and the functional Prss29+ subgroup of gland cells, indicating FOXA2 is obligatory for normal glandular differentiation prior to implantation. We found that this group develops by the evening of day 3 of pregnancy prior to estrogen secretion on day 4 mornings. We noticed that Lif mRNA signals are detected in the uterus comprising the Prss29+ subgroup. Our findings indicate that uterine glands undergo a FOXA2-dependent maturation process to acquire the competence, which we have termed the “transitional phase,” necessary to respond to estrogen. This newly identified glandular "transitional phase" represents a landmark concept in the study of uterine receptivity and implantation biology.
2025-02-15 | GSE275806 | GEO
Project description:Trophoblast Invasion is a complex mechanism that involves several genes and processes that are exquisitely regulated by the mother. Functional genomics has shown that immunomodulatory and proliferation are two essential key processes involved. Adult virgin B6CBA F1/J female mice were mated with CD1 fertile males to induce pregnancy (day 0=vaginal plug). Mice were sacrificed by cervical dislocation. Implantation and inter-implantation sites were divided by sharp dissection 6.5 days post-coitum (dpc) (n=3 mice). Uterine segments included uterine myometrium, stroma, and epithelium. Inter-implantation decidua (ID) were collected and Implantation sites also were divided by sharp dissection to separate extra-embryonic tissue (ET) from surrounding decidua (SD). From the embryo, only the invasive trophoblast formed by the ectoplacental cone was studied too.
2014-06-02 | E-GEOD-46732 | biostudies-arrayexpress
Project description:Gene expression profiling of mouse uterine stromal cells isolated on day 5 of pregnancy
| PRJNA611576 | ENA
Project description:Our study revealed that hypoxia inducible factor 2 alpha, Hif2 alpha, is a downstream target of estrogen signaling in mouse uterine stroma at the time of implantation. Further, conditional deletion of Hif2 alpha in mouse uterus leads to infertility due to impaired epithelial remodeling at the time of implantation. To identify the downstream targets of Hif2 alpha in the uterus, we performed gene expression profiling of uterine stromal cells isolated from Hif2 alpha-intact and -null mice on day 5 of pregnancy, overlapping the window of implantation. The microarray results revealed altered expression of mRNAs corresponding to factors involved in protein trafficking in uterine stroma of Hif2 alpha-ablated mice. These factors mediate crosstalk between uterine storma and epithelial cells to promote epithelial remodeling and implantation. Thus, Hif2 alpha regulates embryo implantation by controlled trafficking of secretory granules during early pregnancy.
2020-07-08 | GSE146650 | GEO