Gene expression signature of endometrial samples from women with and without endometriosis.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA559080 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9915630.fastq.gz | Fastqsanger.gz | |||
| SRR9915640.fastq.gz | Fastqsanger.gz | |||
| SRR9915650.fastq.gz | Fastqsanger.gz | |||
| SRR9915660.fastq.gz | Fastqsanger.gz | |||
| SRR9915670.fastq.gz | Fastqsanger.gz |
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Project description:Endometriosis is a benign gynecological disease characterized by the presence of endometrial-like cells outside the uterus. The prevalence of this disease reaches 10-15% in women of reproductive age which accounts for approximately 200 mln of women worldwide. The existing therapeutic approaches include medications and surgical options, but the risk of post-treatment recurrence of endometriosis remains high. There are currently no effective biomarkers of endometriosis in clinical practice and laparoscopy remains the gold standard for its diagnosis. However, laparoscopy is highly invasive procedure that frequently leads to complications and cannot be used as a routine screening test. In this study we profiled by RNA sequencing 52 endometrial pathological samples and 12 corresponding normal human tissues. We performed two-step differential gene expression analysis of endometrial samples and lesions of patients with endometriosis in comparison with normal reproductive tissues. Based on this analysis we generated a characteristic signature of five genes downregulated in endometriosis with respect to healthy endometrium. The 5-gene expression signature identified had significant predictive power (AUC>0.85) thus suggesting that the marker gene set identified can be used for a low invasive molecular diagnostic of endometriosis. Our data also suggest that the statistical method of five-fold cross validation of differential gene expression analysis procedure can be used for the ability to generate robust gene signatures using real-world clinical data.
2019-10-01 | GSE135485 | GEO
Project description:Alterations in endometrial DNA methylation profile have been proposed as one potential mechanism initiating the development of endometriosis. However, the normal endometrial methylome is influenced by the cyclic hormonal changes and the menstrual cycle phase-dependent epigenetic signature should be considered when studying endometrial disorders. So far, no studies have been performed to evaluate the menstrual cycle influences and endometriosis-specific endometrial methylation pattern at the same time. Therefore, we used Infinium HumanMethylation 450K BeadChip arrays to explore DNA methylation profiles of endometrial tissues from various menstrual cycle phases. Infinium HumanMethylation 450K BeadChip arrays were used to explore DNA methylation profiles of endometrial tissues from mid secretory cycle phase from 17 patients without endometriosis
2016-02-15 | E-GEOD-73949 | biostudies-arrayexpress
Project description:Purpose- To identify the pathways and processes that are dysregulated in the eutopic endometrium of women with endometriosis Methods-RNA sequencing was used to detect and quantify the transcripts encoded by the whole genome in the eutopic endometrium. Mid-secretory phase eutopic endometrial samples from women with (n=4) and without endometriosis (n=4) were processed for RNA sequencing and the data were compared to identify the transcripts displaying differential abundance in women with endometriosis, compared to those without endometriosis (controls)
2021-03-28 | GSE153740 | GEO
Project description:Purpose- To identify the pathways and processes that are dysregulated in the eutopic endometrium of women with endometriosis Methods- RNA sequencing was used to detect and quantify the transcripts encoded by the whole genome in the eutopic endometrium. Mid-proliferative phase eutopic endometrial samples from women with (n=4) and without endometriosis (n=3) were processed for RNA sequencing and the data were compared to identify the transcripts displaying differential abundance in women with endometriosis, compared to those without endometriosis (controls)
2021-03-28 | GSE153739 | GEO
Project description:Endometriosis is a chronic, estrogen-dependent gynecological condition that affects approximately 10% of women of reproductive age. The most widely accepted theory of the etiology of endometriosis includes the process of retrograde menstruation, where menstrual effluent travels up the Fallopian tubes, accesses the peritoneal cavity, and in some people is able to establish endometriotic lesions. Recent reports suggest the uterus is not devoid of bacteria, as was once believed. Thus, the refluxed menstrual effluent may also carry bacteria along with it, and this bacteria has been suggested to contribute to inflammation, and establishment and growth of endometriotic lesions. Here, we sought to compare and contrast the uterine bacteria (endometrial microbiota) in women with surgically confirmed presence or absence of endometriosis using next-generation 16S rRNA gene sequencing. We obtained an average of more than 9000 sequence reads per endometrial biopsy, and found that the endometrial microbiota of women with endometriosis was more diverse (greater Shannon Diversity Index and greater proportion of ‘Other’ taxa) than that of symptomatic controls (women with pelvic pain, but with surgically confirmed absence of endometriosis; diagnosed with other benign gynecological conditions at surgery). The difference in endometrial microbiotas was supported in unsupervised cluster analyses where some clustering of endometrial microbiota by disease status (endometriosis vs. controls) was observed. The bacterial taxa enriched in the endometrial microbiota of women with endometriosis belonged to the Actinobacteria phylum, Oxalobacteraceae and Streptococcaceae families, and Tepidimonas genus, while those enriched in the symptomatic controls (without endometriosis) belonged to the Burkholderiaceae family, and Ralstonia genus. Taken together, our findings suggest the endometrial microbiota is perturbed in people with endometriosis.
2021-04-16 | GSE172172 | GEO
Project description:Alterations in endometrial DNA methylation profile have been proposed as one potential mechanism initiating the development of endometriosis. However, the normal endometrial methylome is influenced by the cyclic hormonal changes and the menstrual cycle phase-dependent epigenetic signature should be considered when studying endometrial disorders. So far, no studies have been performed to evaluate the menstrual cycle influences and endometriosis-specific endometrial methylation pattern at the same time. Therefore, we used Infinium HumanMethylation 450K BeadChip arrays to explore DNA methylation profiles of endometrial tissues from various menstrual cycle phases.
2016-02-15 | GSE73949 | GEO
Project description:Background: Endometriosis affects approximately 10% of reproductive age women and 30%-50% of infertile women. Decreased endometrial receptivity is mainly responsible for infertile women with minimal/mild endometriosis. Medical therapy to improve fecundity of these women is needed. Metformin is reported to inhibit growth of ectopic lesions in endometriosis, while the effect on eutopic endometrium is unclear. The study was to identify if metformin had effect on eutopic endometrium in women with minimal/mild endometriosis and thus improve their fecundity. Materials and Methods: Paired endometrial tissues of secretory phase from participants with minimal/mild endometriosis were collected before and after two months of metformin treatment and setting metformin-free control. Protein expression profiles of endometrium were analyzed by proteomics. Results: A total of 115 proteins were detected up-regulated after metformin therapy, including Insulin-like growth factor-binding protein 7, α-antitrypsin, apolipoprotein D, Rho GDP-dissociation inhibitor 1, brain form glycogen phosphorylase, and Cathepsin B that associated with endometrial receptivity, while there had no significant changes in controls. These up-regulated markers were validated through target proteomics and further demonstrated with endometriosis mice models. Conclusions: This study revealed that metformin might ameliorate biomarkers expressions of endometrial receptivity in human and mice model. Metformin is potential to improve endometrial receptivity of endometriosis-associated infertility.
2021-07-29 | PXD027648 |
Project description:Alterations in endometrial DNA methylation profile have been proposed as one potential mechanism initiating the development of endometriosis. However, the normal endometrial methylome is influenced by the cyclic hormonal changes and the menstrual cycle phase-dependent epigenetic signature should be considered when studying endometrial disorders. So far, no studies have been performed to evaluate the menstrual cycle influences and endometriosis-specific endometrial methylation pattern at the same time. Therefore, we used Infinium HumanMethylation 450K BeadChip arrays to explore DNA methylation profiles of endometrial tissues from various menstrual cycle phases. Infinium HumanMethylation 450K BeadChip arrays were used to explore DNA methylation profiles of endometrial tissues from various menstrual cycle phases from 24 patients with endometriosis
2016-02-15 | E-GEOD-73948 | biostudies-arrayexpress
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
Project description:Eutopic endometrium in endometriosis has molecular evidence of resistance to progesterone (P4) and activation of the PKA pathway in the stromal compartment. To investigate global and temporal responses of eutopic endometrium to P4, we compared early (6-h), intermediate (48-h), and late (14-day) transcriptomes, signaling pathways, and networks of human endometrial stromal fibroblasts (hESFs) from women with endometriosis (hESFendo) to hESFs from women without endometriosis (hESFnonendo). Endometrial biopsy samples were obtained from subjects with and without mild peritoneal endometriosis (n = 4 per group), and hESFs were isolated and treated with P4 (1 μM) plus estradiol (E2) (10 nM), E2 alone (10 nM), or vehicle for up to 14 days. Total RNA was subjected to microarray analysis using a Gene 1.0 ST (Affymetrix) platform and analyzed by using bioinformatic algorithms, and data were validated by quantitative real-time PCR and ELISA. Results revealed unique kinetic expression of specific genes and unique pathways, distinct biological and molecular processes, and signaling pathways and networks during the early, intermediate, and late responses to P4 in both hESFnonendo and hESFendo, although a blunted response to P4 was observed in the latter. The normal response of hESF to P4 involves a tightly regulated kinetic cascade involving key components in the P4 receptor and MAPK signaling pathways that results in inhibition of E2-mediated proliferation and eventual differentiation to the decidual phenotype, but this was not established in the hESFendo early response to P4. The abnormal response of this cell type to P4 may contribute to compromised embryonic implantation and infertility in women with endometriosis. We compared early (6-h), intermediate (48-h), and late (14-day) in vitro whole-genome responses of hESF from women with endometriosis (hESFendo) to hESF from women without endometriosis (hESFnonendo) treated with P4 plus E2 (E2P4), E2 alone, or vehicle alone. Using this experimental paradigm, the data demonstrate unique phenotypes, gene expression processes, biochemical and signaling pathways, and networks suggestive of early, intermediate, and late responses of hESFnonendo and hESFendo to P4, giving insights into the complexity of events occurring normally in response to P4 and in the setting of endometriosis.
2012-01-24 | E-GEOD-35287 | biostudies-arrayexpress