Estrogen Receptor beta cistrome in mouse endometriotic tissue.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE114047 | GEO | 2019/09/12
REPOSITORIES: GEO
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Project description:The Estrogen Receptor beta (ERβ) has an essential role in endometriosis progression. However, the molecular mechanism of how ERβ drives endometriosis progression is not elucidated, yet. To define the role of genomic ERβ in endometriosis progression, we have employed whole-genome microarray expression profiling as a discovery platform to identify ERβ-regulated transcriptome in endometriotic tissues. To get this transcriptome, we applied endometrium specific ERβ overexpression (ERBOE) mouse model by crossing mouse having a pCAG promoter-loxPSTOPloxP-ERβ cassette with PRCre knockin mice that Cre recombinase cDNA was inserted into exon 1 of PR gene. Endometriosis was surgically induced in ERBOE mice and PRCre mice as the control by transplantation of uterine tissues. The ectopic lesions and eutopic endometrium were harvested at the estrus cycle in 4th weeks after endometriosis induction.
2019-09-12 | GSE114010 | 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:miRNA high-throughput sequencing was used to investigate endometriosis lesion-specific miRNA expression profiles by comparing a set of paired samples of peritoneal endometriotic lesions and matched healthy surrounding tissue together with eutopic endometrium of the same patients. We found that miRNAs of surrounding peritoneal tissue mask most of the miRNA expression differences that could originate from endometriotic tissue and thus only miRNAs with significantly different levels in the endometriotic lesions compared to peritoneal tissue were detected. According to the results of this study, two miRNAs – miR-34c and miR-449a showed remarkably higher expression in lesions compared to healthy tissue.
2015-01-06 | GSE56414 | 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. 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:Estrogen Receptor beta cistrome in mouse endometriotic tissue.
| PRJNA464028 | ENA
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 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
Project description:Endometriosis is a common gyncological disease that affects 10-20% of women in child-bearing age. It is defined by the presence of endometrial tissues outside the uterus. The causes remain elusive, but the endometrium of these patients differs profoundly from that of disease-free subjects. During pregnancy, the maternal-fetal interface is built onto decidualized endometrium. We investigated whether this interface is normal when the subjects suffer of endometriosis and showed remarkly properties of eutopic endometrium from endometriosis-affected women to spontaneously develop endometriotic-like lesions within direct contact to non-uterine tissues.
2014-11-10 | GSE57733 | GEO
Project description:Endometriosis is a common gynecological disease that affects 10-20% of women in child-bearing age. It is defined by the presence of endometrial tissues outside the uterus. The causes remain elusive, but the endometrium of these patients differs profoundly from that of disease-free subjects. During pregnancy, the maternal-fetal interface is built onto decidualized endometrium. We investigated whether this interface is normal when the subjects suffer of endometriosis and showed remarkly properties of eutopic endometrium from endometriosis-affected women to spontaneously develop endometriotic-like lesions within direct contact to non-uterine tissues.
2014-11-10 | GSE57831 | GEO
Project description:Endometriosis is associated with aberrant gene expression in the eutopic endometrium of women with disease. To determine if the development of endometriotic lesions directly impacts eutopic endometrial gene expression, we sequentially analyzed the eutopic endometrium across the time course of disease progression in a baboon model of induced disease. Endometriosis was induced in baboons by intraperitoneal inoculation of autologous menstrual endometrium. Eutopic endometria were collected at 9-11 days postovulation) in five time points: 1, 3, 6-7, 10-12, and 15-16 months after disease induction and compared with tissue from disease-free baboons. We used microarrays to identify differentially expressed genes between time points. Sequential analysis of the same animals during disease progression demonstrated an early disease insult and a transitory dominance of an estrogenic phenotype. However, as the disease progressed, a progesterone-resistant phenotype became evident. Endometriosis was experimentally induced in Papio anubis female baboons (n = 4) by intraperitoneal inoculation with menstrual endometrium on two consecutive menstrual cycles. Baboons with spontaneous endometriosis (n = 2) were also included in this study with an unknown duration of disease. Control endometrium was similarly harvested from animals (n = 4) with no previous surgeries and with no visible disease. The progression of disease was monitored in each animal by consecutive laparoscopies and video recording at 1 (n = 2), 3 (n = 4), 6-7 (n = 4), 10-12, (n = 4), and 15-16 (n = 3) months after inoculation during a window of 9-11 days postovulation. Eutopic endometrial tissues were harvested and were snap frozen in liquid nitrogen for RNA extraction. Additionally, menstrual endometrium was harvested on Days 1-2 of menses using a Unimar Pipelle (Cooper Surgical Inc., Shelton, CT) immediately prior to laparoscopy. Blood samples were collected daily from days 7 through 16 postmenstruation of menstrual cycles.
2015-08-27 | E-GEOD-72428 | biostudies-arrayexpress