Endometriotic lesions exert distinct metabolic activity compared to paired eutopic endometrium at a single-cell level
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1040179 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26824401_1.fastq.gz | Fastqsanger.gz | |||
| SRR26824401_2.fastq.gz | Fastqsanger.gz | |||
| SRR26824402_1.fastq.gz | Fastqsanger.gz | |||
| SRR26824402_2.fastq.gz | Fastqsanger.gz | |||
| SRR26824403_1.fastq.gz | Fastqsanger.gz |
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Project description:Eutopic endometrium (EuE) and endometriotic peritoneal lesions (ectopic endometrium, EcE) are heterogenous tissues according to the recent scRNA studies. We aimed to explore metabolic profile of cell populations in paired samples of EuE and EcE from four women with endometriosis. We found changes in the regulation of progesterone and estradiol signaling pathways in perivascular, stromal and endothelial cells of EcE compared to EuE, which might have a direct effect on cellular metabolism and contribute to cell proliferation and angiogenesis. The metabolic pathways were differentially regulated in perivascular, stromal and endothelial clusters, and metabolic pathway activity change between EcE and EuE was the highest for AMPK, HIF-1, glutathione metabolism, OXPHOS, and glycolysis/ gluconeogenesis. Remarkably, we identified co-activation of glycolysis and OXPHOS in perivascular and stromal cells of EcE compared to EuE. Previous studies reported a Warburg-like effect in endometriosis with a high use of glycolysis pathway over oxidative metabolism. Our observations might suggest the employment of both OXPHOS and glycolysis to meet the energy demands of proliferating cells in endometriotic lesions.
2024-07-21 | GSE247695 | GEO
Project description:The mechanisms underlying the pathophysiology of endometriosis, characterized by the presence of endometrium-like tissue outside the uterus, remain poorly understood. This study aimed to identify cell type-specific gene expression changes in superficial peritoneal endometriotic lesions and elucidate the crosstalk among the stroma, epithelium, and macrophages compared to patient-matched eutopic endometrium. Surprisingly, comparison between lesions and eutopic endometrium revealed transcriptional similarities, indicating minimal alterations in the sub-epithelial stroma and epithelium of lesions. Spatial transcriptomics (NanoString GeoMx) highlighted increased signaling between the lesion epithelium and macrophages, emphasizing the role of the epithelium in driving lesion inflammation. We propose that the superficial endometriotic lesion epithelium orchestrates inflammatory signaling and promotes a pro-repair phenotype in macrophages, providing a new role for Complement 3 in lesion pathobiology. This study underscores the significance of considering spatial context and cellular interactions in uncovering mechanisms governing disease in endometriotic lesions.
2024-04-16 | GSE263897 | GEO
Project description:The pathophysiology of endometriotic lesion development remains unclear but involves a complex interaction between ectopic endometrium and host peritoneal tissues. We hypothesised that disruption of this interaction was likely to suppress endometriotic lesion formation. We hoped to delineate the molecular and cellular dialogue between ectopic human endometrium and peritoneal tissues in nude mice, as a first step towards testing this hypothesis. Human endometrium was xenografted into nude mice and the resulting lesions were analysed using microarrays. A novel technique was developed that unambiguously determined whether RNA transcripts identified by the microarray analyses originated from human cells (endometrium) or mouse cells (stroma). Four key pathways (ubiquitin/proteosome, inflammation, tissue remodelling/repair and ras-mediated oncogenesis) were revealed, that demonstrated communication between host stromal cells and ectopic endometrium. Experiment Overall Design: Paired samples of eutopic and ectopic endometrium from 9 individual women were collected and the transcript profiles compared.
2009-01-02 | E-GEOD-11691 | biostudies-arrayexpress
Project description:The pathogenesis of endometriosis may result from aberrant angiogenesis that occurs in eutopic endometrium with retrograde menstruation. The difference in gene expression profile between human endometrial endothelial cells (HEECs) from eutopic endometria of patients with and without endometriosis would be determinant that affects the occurrence of endometriosis. To explore this kind of difference, we performed in vitro culture and identified their endothelial origin, as well as observed growth features of HEECs from the two different origins. Finally we identified the difference in gene expression profile when combined suppression subtractive hybridization(SSH) with genechip and confirmed the results by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The HEECs derived from endometriosis exhibited potent survival ability in vitro compared to that from non-endometriosis. We found that gremlin and fibronectin genes were up-regulated in HEECs derived from eutopic endometrium of patients with endometriosis when compared with that from patients without endometriosis. Our study implies that enhanced angiogenic capacity of eutopic HEECs may be an independent determinant in endometriotic aberrant angiogenesis in addition to the interaction of exfoliated endometrium and peritoneal environment elements such as activated macrophages and soluble cytokines. Experiment Overall Design: We analyzed 5 arrays for HEECs derived from eutopic endometrium of patients with endometriosis and 5 arrays for HEECs derived from that of patients without endometriosis
2008-06-15 | E-GEOD-7846 | biostudies-arrayexpress
Project description:Brief description of the experiment: The objective of this experiment was to use DNA microarrays to identify differentially expressed genes in eutopic uterine endometrium compared to ectopic endometrium. 174 of the 53,000 genes on the whole human DNA microarrays were changed by 5-fold or greater in ectopic vs. eutopic endometrium. Families of genes that were differentially expressed include immune system and inflammatory pathway genes, genes whose cognate proteins code for cell adhesion, junctional proteins, the extracellular matrix and its remodeling, and cytoskeletal proteins, and ligands, receptors, and components of specific signal transduction pathways. The altered immune environment may allow survival of endometriotic cells that enter the peritoneal cavity. Alterations of cell adhesion-associated genes may contribute to the adhesive and invasive properties of ectopic endometrium, and changes in signal transduction pathways support a change in the communication among cells of the endometrial explant compared to eutopic endometrium. These families of differentially expressed genes provide multiple opportunities for the development and testing of new hypotheses regarding endometriosis. Keywords: disease state analysis, endometriosis
2007-02-15 | GSE5108 | GEO
Project description:Comparison of macrophages M1 (M1) and M2 (M2) from eutopic endometrium from women with and without endometriosis
2020-01-22 | GSE130435 | GEO
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
Project description:Current therapeutics of endometriosis focus on hormonal disruption of endometriotic lesions (ectopic endometrium, EcE). Recent findings show higher glycolysis utilization in EcE, suggesting non-hormonal strategy for disease treatment that addresses cellular metabolism. Identifying metabolically altered cell types in EcE is important for targeted metabolic drug therapy without affecting eutopic endometrium (EuE). Here, using single-cell RNA-sequencing, we examine twelve metabolic pathways in paired samples of EuE and EcE from women with confirmed endometriosis. We detect nine major cell types in both EuE and EcE. Metabolic pathways are most differentially regulated in perivascular, stromal, and endothelial cells, with the highest changes in AMPK signaling, HIF-1 signaling, glutathione metabolism, oxidative phosphorylation, and glycolysis. We identify transcriptomic co-activation of glycolytic and oxidative metabolism in perivascular and stromal cells of EcE, indicating a critical role of metabolic reprogramming in maintaining endometriotic lesion growth. Perivascular cells, involved in endometrial stroma repair and angiogenesis, may be potential targets for non-hormonal treatment of endometriosis.
| S-EPMC11339455 | biostudies-literature
Project description:In this study, we performed transcriptomic analysis in ectopic lesions and eutopic endometrial tissues from both fertile and subfertile mice with endometriosis. We identified the positive correlation of the gene signatures between the mouse and human in ectopic lesions. Conserved gene networks were activated in all the ectopic lesions including estradiol, immune, fibrosis, and angiogenesis pathways. The interactions mediated through hormone, cytokine, and growth factor as well as their corresponding receptors were predicted between the ectopic and eutopic endometrium. EGF and WNT signaling were more suppressed in the eutopic endometrium from subfertile mice. Our results revealed that our mouse endometriosis model recapitulates the important transcriptomic changes of endometriosis progression in human ectopic lesions including the essential regulator network and intensive inter-communications between ectopic and eutopic endometrium. Our preclinical animal model for endometriosis will be invaluable to understand etiology and pathophysiology on endometriosis.
2024-05-29 | GSE240392 | GEO
Project description:The pathogenesis of endometriosis may result from aberrant angiogenesis that occurs in eutopic endometrium with retrograde menstruation. The difference in gene expression profile between human endometrial endothelial cells (HEECs) from eutopic endometria of patients with and without endometriosis would be determinant that affects the occurrence of endometriosis. To explore this kind of difference, we performed in vitro culture and identified their endothelial origin, as well as observed growth features of HEECs from the two different origins. Finally we identified the difference in gene expression profile when combined suppression subtractive hybridization(SSH) with genechip and confirmed the results by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The HEECs derived from endometriosis exhibited potent survival ability in vitro compared to that from non-endometriosis. We found that gremlin and fibronectin genes were up-regulated in HEECs derived from eutopic endometrium of patients with endometriosis when compared with that from patients without endometriosis. Our study implies that enhanced angiogenic capacity of eutopic HEECs may be an independent determinant in endometriotic aberrant angiogenesis in addition to the interaction of exfoliated endometrium and peritoneal environment elements such as activated macrophages and soluble cytokines. Keywords: human endometrial endothelial cells (HEECs),endometriosis,differentially expressed genes
2007-10-31 | GSE7846 | GEO