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Overactivation of notch1 signaling in uterine epithelium

ABSTRACT: Overactivation of notch1 signaling in uterine epithelium

PROVIDER: PRJNA851759 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19783912.fastq.gz	Fastqsanger.gz
	SRR19783913.fastq.gz	Fastqsanger.gz
	SRR19783914.fastq.gz	Fastqsanger.gz
	SRR19783915.fastq.gz	Fastqsanger.gz
	SRR19783916.fastq.gz	Fastqsanger.gz

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Overactivation of notch1 signaling in uterine epithelium

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Aberrant activation of canonical Notch1 signaling in the mouse prostate drives epithelialcell proliferation and induces prostatic hyperplasiaby increasing androgen receptor sensitivity

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Gene expression profiling of mouse luminal uterine epithelium with knockout of ALK3

Project description:Bone morphogenetic proteins (BMPs) are transforming growth factor Î² (TGFÎ²) family members that regulate the post-implantation and mid-gestation stages of pregnancy. In this study we discovered that signaling via activin-like kinase 3 (ALK3/BMPR1A), a BMP type 1 receptor, is necessary for blastocyst attachment. To understand the role of ALK3 in the luminal uterine epithelium, we obtained the gene expression profiles of isolated luminal uterine epithelium from 3.5dpc control and Alk3 cKO mice. Gene expression profiling of isolated luminal uterine epithelium from control and Alk3 cKO mice. two group comparison

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Project description:We used the microarray analysis to determine the differential gene expression profiles in mouse uterine luminal epithelium between preimplantation gestation day 3.5 and postimplantation gestation day 4.5, and investigeate the molecular mechanism of the establishment of uterine receptivity and embryo implantation. Uterine luminal epithelium (LE) is critical for the establishment of uterine receptivity during embryo implantation. Many genes are known to have differential expression in the periimplantation LE but the global profiling of the altered genes in the periimplantation LE is unknown. To fill in this knowledge gap, microarray analysis was performed in gestation day 3.5 (D3.5, preimplantation) and D4.5 (postimplantation) mouse LE from natural pregnancy. There were 382 significantly upregulated and 245 significantly downregulated genes (>2 fold, P<0.05) in the D4.5 LE. There are 6 samples. 3 for gestation day 3.5 uterine luminal epithelium, the other 3 for gestation day 4.5 uterine luminal epithelium

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Constitutive expression of Progesterone Receptor B in the uterine epithelium prevents implantation by inhibiting estrogen regulation of LIF signaling [RNAseq-PRAoe_PRBoe_oil_P4]

Project description:RNA-seq analysis of uterine luminal epithelium at D4.5 indicates that epithelial PGRA and PGRB shares conseved pathways. Constitutive epithelial PGRA and PGRB disrupts the embryo implantation both through the suppressed FOXO1 signaling by excluding FOXO1 from the nuclear at the uterine epithelium. There are three layers of regulation. Firstly, PGRA and PGRB diminishes Lif transcription in uterine glands by blocking ESR1 binding at the Lif promoter at D3.5 which is critical for the FOXO1 nuclear expression at D4.5 through LIF/pSTAT3/FOXO1. Secondly, PGRA and PGRB directly suppres Foxo1 transcription at the uterine epithelium probably through direct binding at Foxo1 promoter. Thirdly, PGRA and PGRB promotes the Sgk1 transcription, the kinases that phosphorylate FOXO1 to translocate it into cytoplasma for degradation.

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Expression data from in vitro decidualized human uterine fibroblast cells (HuF cells) with or without NOTCH1 silencing

Project description:Decidualization is a critical process for embryo implatation during which uterine stromal fibroblasts are transformed into large, epithelioid-like decidual cell. NOTCH1 is recepotor of Notch signaling that plays important roles for cell-cell communication, which involves gene regulatory mechanisms that control multiple cellular differentiation processes during embryonic and adult life. Here we silenced NOTCH1 by shRNA in HuF cells and studied how it affects decidualization HuF cells were cultured, transfected with NOTCH1 shRNA via a lentivirus system, following by a in vitro induced decidualization by EPC cocktail (36 nM estradiol-17Î² and 1 Î¼M medroxyprogesterone acetate, and 0.1 mM dbcAMP) for 6 days. RNAs were extracted then hybridized on Affymetrix microarrays. There are four experimental conditions: 1) transfected with empty plasmid; 2) transfected with hNOTCH1 lentiviral-shRNA plasmid; 3) transfected with empty plasmid and treated with EPC cocktail; and 4) hNOTCH1 lentiviral-shRNA plasmid with subsequent treatment of EPC cocktail. HuF cells from two different patients were used in each group (HuF86P4 & HuF88P4).

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