Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

EGR1-controlled transcriptome of T HESCs

ABSTRACT: Sequencing of mRNA isolated from a human endometrial stromal cell line (T HESCs) following control or EGR1 siRNA-mediated knockdown.

ORGANISM(S): Homo sapiens

PROVIDER: GSE123472 | GEO | 2019/04/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

EGR1-controlled transcriptome of T HESCs

Project description:EGR1-controlled transcriptome of T HESCs

| PRJNA508815 | ENA

EGR1 genomic binding in t-HESC cell line

Project description:Whole genome binding profile of EGR1 in human endometrial stromal cells

2019-11-26 | GSE141063 | GEO

Gene expression changes in primary human endometrial stromal cells following METTL3 knockdown during in vitro decidualization

Project description:We developed an in vitro model in which primary human endometrial stromal cells (HESCs) were induced to differentiate through treatment with MPA and 8-Br-cAMP. SiRNA-mediated knockdown of METTL3 was performed on HESCs, 6 h prior to treatment of 8-Br-cAMP and MPA.

2024-04-14 | GSE263330 | GEO

EGR1 regulation in human bone marrow stromal cells

Project description:Human bone marrow stromal cells (BMSCs) are key elements of the hematopoietic environment and they play a central role in bone and bone marrow physiology. However, how key BMSC functions are regulated is largely unknown. We analyzed the role of the immediate early response transcription factor EGR1 as key BMSC regulator and found that EGR1 was highly expressed in prospectively-isolated primary BMSCs, downregulated upon culture, and lower in non-CFU-F-containing CD45neg BM cells. Furthermore, EGR1 expression was lower in proliferative regenerating adult and fetal primary cells compared to adult steady-state BMSCs. Accordingly, EGR1 overexpression markedly decreased BMSC proliferation but considerably improved hematopoietic stroma support function as indicated by an increased production of transplantable CD34+CD90+ hematopoietic stem cells in expansion co-cultures. The improvement of BMSC stroma support function was mediated by increased expression of hematopoietic supporting genes, such as VCAM1 and CCL28. On the other hand, EGR1 knockdown increased ROS-mediated BMSC proliferation, and clearly reduced BMSC hematopoietic stroma support potential. These findings thus show that EGR1 is a key BMSC transcription factor with a dual role in regulating proliferation and hematopoietic stroma support function that is controlling a genetic program to coordinate the specific functions of BMSC in their different biological contexts.

2019-06-27 | PXD011767 | Pride

COUP-TFII regulates human endometrial stromal genes involved in inflammation

Project description:Although the function of COUP-TFII in uterine decidualization has been described in mice, its role in the human uterus remains unknown.To interrogate the role of COUP-TFII in human endometrial function, we utilized a siRNA-mediated loss of function approach in primary human endometrial stromal cells. Primary human endometrial stromal cells (HESCs), coup-TFII siRNA group and control group Two group comparison

2014-01-07 | E-GEOD-47052 | biostudies-arrayexpress

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

PER2 synchronizes mitotic expansion and decidual transformation of human endometrial stromal cells

Project description:Implantation is dependent on synchronized interactions between the conceptus and surrounding decidual cells but the involvement of clock genes in this process is not well understood. Circadian oscillations are predicated on transcriptional-translational feedback loops, which balance the activities of the transcriptional activators CLOCK and BMAL1 and repressors encoded by PER and CRY genes. Here we show that loss of PER2 expression silences circadian oscillations in decidualizing human endometrial stromal cells (HESCs). Downregulation was preceded by reduced CLOCK binding to a noncanonical E-box enhancer in the PER2 promoter and occurred between 12 - 24 h after exposure to a deciduogenic stimulus. RNA sequencing revealed that premature inhibition of PER2 by siRNA knockdown leads to a grossly disorganised decidual response. Gene ontology analysis highlighted a preponderance of cell cycle regulators amongst the 1,121 genes perturbed upon PER2 knockdown. Congruently, PER2 inhibition abrogated mitotic expansion of differentiating HESCs by inducing cell cycle block at G2/M. Analysis of mid-luteal endometrial biopsies revealed an inverse correlation between PER2 transcript levels and the number of miscarriages in women suffering reproductive failure. Thus, PER2 synchronizes mitotic expansion of HESCs with a periodic decidual gene expression; uncoupling of these events may cause persistent pregnancy failure. Endometrial mRNA profiles of paired control (siRNA-NT) and siRNA-PER2 were generated by deep sequencing, in triplicate using Illumina

2015-09-16 | E-GEOD-62854 | biostudies-arrayexpress

GOLPH3 modulates expression and alternative splicing of transcription factors associated with endometrial decidualization in human endometrial stromal cells

Project description:GOLPH3 was silenced in human endometrial stromal cells (hESCs), and the transcriptome data (RNA-seq) by GOLPH3 knockdown (siGOLPH3) was obtained by high-throughput sequencing technology,

2022-10-12 | GSE215155 | GEO

The Promyelocytic Leukemia Zinc Finger Dependent Transcriptome during Human Endometrial Stromal Cell Decidualization

Project description:RNA-sequencing of mRNA isolated from in vitro decidualizaing human endometrial stromal cells with or without siRNA-mediated knockdown of PLZF

2018-03-29 | GSE112362 | GEO

Evolutionary transcriptomics of Eutherian gene expression gains and the origins of decidualization [Set 7]

Project description:We used human endometrial stromal fibroblast cell line to perform an siRNA knockdown coupled with RNA-seq screen of a series of transcription factors that gained expression in the endometrial tissue of Eutherian mammals.

2022-02-28 | GSE189645 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data