Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Pyroptotic T-cell-derived active IL-16 has a driving function in endometriosis development

ABSTRACT: Endometriosis is a common, chronic inflammatory condition that frequently results in pain and infertility and is estimated to affect 6–10% of women of reproductive age. However, the mechanisms underlying the induction of inflammation in endometriosis remain unclear. Here, we identified that ectopic endometrial T-cell-derived active interleukin (IL)-16 acts as an inflammation-driving cytokine in endometriosis. Furthermore, we found that in ectopic endometrial T cells, the activation of IL-16 requires iron overload-induced caspase-3 activity and that the release of active IL-16 is reliant on GSDME-mediated pyroptosis. These observations suggest that active IL-16 may represent a promising target in the treatment of endometriosis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE229735 | GEO | 2024/04/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Proteomics of ectopic endometrial cell-derived exosomes in endometriosis

Project description:We primary cultured ectopic endometrial cells from patients with endometriosis (2 cases) and without endometriosis(2 cases) and collected cell culture supernatants（P0). We isolated exosomes from cell culture supernatants by differential centrifugation and then performed proteome analysis on the two groups of exosomes to investigate the role of ectopic endometrial cell-derived exosomes in the development of endometriosis.

2022-06-09 | PXD033124 | Pride

Deep quantitative proteomics underlies extensive metabolic reprogramming and cancer-like changes of ectopic endometriotic stromal cells

Project description:Endometriosis is a prevalent health condition in women of reproductive age characterized by ectopic growth of endometrial tissue in the extrauterine environment. Thorough understanding of the molecular mechanisms underlying the disease are still lacking and incomplete. We dissect eutopic and ectopic endometrial primary stromal cell proteomes to a depth of nearly 6900 proteins using quantitative mass-spectrometry with a spike-in SILAC standard. Acquired data reveal metabolic reprogramming of ectopic stromal cells of endometriosis with extensive upregulation of glycolysis and down-regulation of oxidative respiration – a wide-spread metabolic phenotype previously described in many cancers. Our results also underlie other molecular changes of ectopic endometriotic stromal cells indicating reduced apoptotic potential, increased cellular adhesiveness/invasiveness and altered immune function. The changes related to metabolism are additionally reflected by attenuated aerobic respiration of ectopic endometrial stromal cells measured by live cell oximetry and by altered mRNA levels. These comprehensive proteomics data refine the current understanding of endometriosis presenting potential new avenues for therapies.

2015-12-21 | PXD002845 | Pride

Deep quantitative proteomics underlies extensive metabolic reprogramming and cancer-like changes of ectopic endometriotic stromal cells

2016-10-22 | MSV000080276 | MassIVE

Genome-wide DNA methylation profiling in cultured eutopic and ectopic endometrial stromal cells (expression)

Project description:Transcriptome profiles were investigated in isolated endometrial stromal cells (ESCs) from eutopic and ectopic endometrium. The profiles were quite different between eutopic ESC and ectopic ESC, whereas no clear dfference was recognized between eutopic ESC with and without endometriosis. Total RNA from three cultured endometrial stromal cells (ESCs) from eutopic endometria without endometriosis, three ESCs with endometriosis and three ESCs from chocolate cysts were hybridised to the Affymetrix Human Gene 1.0 ST Array.

2013-09-07 | E-GEOD-47360 | biostudies-arrayexpress

Genome-wide DNA methylation profiling in cultured eutopic and ectopic endometrial stromal cells (methylation)

Project description:Profiles of genome-wide DNA methylation were investigated in isolated endometrial stromal cells from eutopic and ectopic endometrium. DNA methylation profiles were quite different between eutopic ESC and ectopic ESC, whereas no clear dfference were recognized between eutpic ESC with and without endometriosis. Bisulphite converted DNA from three cultured endometrial stromal cells (ESCs) from eutopic endometria without endometriosis, three ESCs with endometriosis and three ESCs from chocolate cysts were hybridised to the Illumina infinium HumanMethylation27 BeadChip.

2013-09-07 | E-GEOD-47359 | biostudies-arrayexpress

Gene expression profiling of SF1 in mouse uterus tissues

Project description:Epigenetic silencing of Steroidogenic Factor 1 (SF1) is lost in endometrial tissue in endometriosis and this is hypothesized to result in de novo local steroidogenesis favoring growth and inflammation. The goal of this study was to evaluate the endometrial specific transcriptional and functional role of SF1 in vivo by utilizing a mouse model in which SF1 was conditionally expressed in the uterus. SF1 expression resulted in the development of cystic endometrial glands and infertility. Endometriosis induction by auto-transplantation of a biopsy of uterine tissue sutured to the mesenteric membrane resulted in 4-fold increase in size ectopic lesions from SF1 expressing mice. Microarray analysis demonstrated SF1-regulated genes are involved in several pathways including epithelial and tube development, migration of lymphocytes and leukocytes, cellular movement and vascular development. experimental group (SF-1 transgenic) and control group

2016-04-14 | E-GEOD-66963 | biostudies-arrayexpress

Differential expression of microRNAs between eutopic and ectopic endometrium in ovarian endometriosis

Project description:Endometriosis is defined as the presence of endometrial tissue (eutopic tissue) outside the uterus (ectopic tissue). We assessed differentially expressed microRNAs in ectopic endometrium compared with eutopic endometrium. Comparison of paired eutopic/ectopic endometrium microRNAs from three patients.

2010-12-30 | E-GEOD-26346 | biostudies-arrayexpress

Differential expression of microRNAs between eutopic and ectopic endometrium in ovarian endometriosis

2010-12-30 | GSE26346 | GEO

The differential expression of mRNAs and long noncoding RNAs between ectopic and eutopic endometrium of adenomyosis

Project description:Adenomyosis, defined as ectopic endometrial tissue within the myometrium, can often be misdiagnosed as multiple uterine leiomyomata or endometrial thickening. We therefore performed a combined mRNA and long noncoding (lnc)RNA microarray and bioinformatic analysis of eutopic and ectopic endometrium in women with adenomyosis to better understand its pathogenesis and help in the development of a semi-invasive diagnostic test. A total of 586 mRNAs were increased and 305 mRNAs decreased in ectopic endometrium of adenomyosis compared with eutopic endometrium, while 388 lncRNA transcripts were up-regulated and 188 down-regulated in ectopic compared with paired eutopic endometrial tissue. Bioinformatic analysis suggested a series of metabolic and molecular abnormalities in adenomyosis, which have many similarities with endometriosis. Furthermore, our study constitutes the first known report of lncRNA expression patterns in human adenomyosis ectopic and eutopic endometrial tissue. Two-condition experiment, ectopic endometrium vs. eutopic endometrium. 3 samples,self-control

2015-10-28 | E-GEOD-74373 | biostudies-arrayexpress

Gene expression profiling of SF1 in mouse uterus tissues

2016-04-14 | GSE66963 | 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