Microvascular Permeability, Inflammation, and Lesion Physiology in Endometriosis: A Microphysiological Systems Approach
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PROVIDER: PRJNA987021 | ENA |
REPOSITORIES: ENA
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Project description:Microvascular Permeability, Inflammation, and Lesion Physiology in Endometriosis: A Microphysiological Systems Approach
| PRJNA987020 | ENA
Project description:We performed gene expression analysis human peritoneal endometriosis lesions, eutopic endometrium from endometriosis patients and peritoneum form endometriosis patients.The goal of the study was to analyse gene expression differences between peritoneal endometriosis lesion and eutopic endometrium and peritoneal endometriosis lesion and peritoneum.
2012-12-06 | E-MTAB-694 | biostudies-arrayexpress
Project description:Our understanding of molecular mechanisms contributing to the pathophysiology of endometriosis, and their upstream regulators, remains limited. Using a C57Bl/6 mouse model of endometriosis in which decidualized endometrial tissue fragments are transferred to subcutaneous sites in recipient mice to mimic endometriosis lesions, we have generated a comprehensive profile of gene expression in decidualized endometrial tissue (n=4), and endometriosis-like lesions at Day 7 (n=4) and Day 14 (n=4) of lesion formation. High throughput mRNA sequencing allowed identification of genes and pathways involved in the initiation and progression of endometriosis-like lesions. We found distinct patterns of gene expression with substantial differences between the lesions and the decidualized endometrium from which they arose, but no differentially expressed genes between the two lesion timepoints. The transcriptional changes at the outset of lesion formation indicated substantial upregulation of immune response-associated canonical pathways. Pathway enrichment analysis indicates multiple potential endogenous upstream regulators, and reveals multiple gene candidates not previously implicated in endometriosis lesion formation suggesting these mediators may have novel roles in disease progression. Collectively, the provided data will be a valuable resource to inform research on the molecular mechanisms contributing to endometriosis development.
2024-10-17 | GSE255418 | GEO
Project description:A Human iPSC-derived Microphysiological Blood-Brain Barrier Model for Permeability Screening
| PRJEB36737 | ENA
Project description:Endometriosis is a benign gynecological condition that causes significant morbidity due to reduced fertility, pelvic pain and inflammatory dysfunctions. High-fat dietary intake has been linked to higher systemic inflammation and oxidative stress, which are both features of women with endometriosis. We evaluated the effects of high-fat diet (HFD) on endometriosis progression using immunocompetent mouse model wherein ectopic lesion was induced in wildtype and kruppel-like factor 9 (KLF9)- null donor mice. Results showed that HFD leads to increased ectopic lesion numbers and higher body weight gain. The HFD-promotion of lesion establishment was associated with decreased stromal estrogen receptor 1 and progesterone receptor expression, increased macrophage infiltration, and enhanced expression of pro-inflammarory and pro-oxidative stress pathway genes. Further, lesion-bearing mice had higher peritoneal fluid TNF-α and elevated local/systemic redox status than control-fed mice.
2017-04-23 | GSE80603 | GEO
Project description:Introduction: Endometriosis is a debilitating condition where endometrial-like tissue grows outside the uterus and rarely in distant sites such as the lungs, heart and brain. Symptoms are severe chronic pain, bladder/bowel problems, painful sex and infertility. Differences in endometrium between women with and without endometriosis have not been constructive, and there is still paucity in its pathogenesis and non-invasive diagnostic test, leading to delayed diagnosis (~10 years) and effective treatment. Menstrual fluid (MF) gives a peak into endometrial health. Could MF extracellular vesicles (EVs) point to the pathogenesis and a non-invasive diagnostic tool for endometriosis? Aims: To identify differences in protein-cargo in MF-EVs from women with and without endometriosis, define their functional contribution to mesothelial niche cells for lesion establishment and determine whether MF-sEV can be a non-invasive endometriosis diagnostic tool. Methods: MF was collected from women with and without endometriosis on day 2 of menses and EVs isolated using differential centrifugation. MF-EVs were identified by size, morphology and protein markers and subjected to TMT- quantitative proteomics assay. Differentially expressed proteins were analysed. Ctrl and Endo MF-sEV were co-cultured with mesothelial cells to assess for uptake and changes in the adhesive and junctional proteins. Results: Spherical-shaped MF-EVs were identified with mean diameters of 121.9 nm (Endo) and 123.8 nm (Ctrl), expressing TSG101, Alix and Syntenin-1 sEV proteins. MF-sEV proteins originated from endometrial cells: stem cells, leucocytes, and endothelial and smooth muscle cells, validating the endometrial origin of the MF-EVs. 77% of identified proteins were differentially expressed. In endo-MF-sEV, proteins regulating HGF receptor (anoikis), cellular senescence and multiple apoptotic, nitrogen compound metabolic processes and TRP channels signalling (immunity and contraction regulation) were decreased, potentially promoting lesion establishment, survival and pain. Similarly, antibacterial peptides (cathelicidin, mucin-1, lipocalin2 and serum amyloid A) were downregulated. The majority of proteins were significantly downregulated in endometriosis suggesting a dysregulation in the protein synthesis and cellular communication for homeostasis. Two-thirds of upregulated proteins were immunoglobulins indicating inflammatory pathogenesis. This was reflected by an increased Endo-MF-EVs uptake by mesothelial cells, with decreased scribble resulting in decreased cellular resistance and permeability. Conclusions: MF-EVs contain vital information indicative of endometriosis pathogenesis and may be the key to developing a simple and early diagnostic tool.
2025-05-06 | PXD042101 | Pride
Project description:Endometriosis, a benign inflammatory disease whereby endometrial-like tissue grows outside the uterus, is a risk factor for endometriosis-associated ovarian cancers. In particular, ovarian endometriomas, cystic lesions of deeply invasive endometriosis, are considered the precursor lesion for ovarian clear-cell carcinoma (OCCC). To explore the transcriptomic landscape, OCCC from women with pathology-proven concurrent endometriosis (n = 4) were compared to benign endometriomas (n = 4) by bulk RNA and small-RNA sequencing.
2023-07-29 | GSE230956 | GEO
Project description:Endometriosis in mice and association with dysbiosis during the acute phase of lesion formation
| PRJEB32559 | ENA
Project description:Endometriosis -associated ovarian carcinoma (EAOC) is mostly malignant transformation from endometriomas. However, the endometriosis cancerogenesis remains to be established. Using spatial transcriptomic of human specimens of normal, endometriomas and EAOC, activation of Interleukin-17C (IL-17C) signaling is identified, with higher IL-17 receptor E (IL-17RE) expression in endometriotic cells, to be associated with cancerogenesis and which has no previous association with EAOC. Elevated IL-17C concentration is found in peritoneal fluid in women with ovarian cancer and IL-17RE-overexpressed endometriosis mice. In particular, IL-17C knockout reduces peritoneal fluid IL-17C concentration and inhibits ectopic lesion growth in endometriosis mice. Besides, the role of IL-17C in the endometriosis cancerogenesis was investigated by blocking the IL-17C/IL-17RE, modulating IL-17RE and neutralizing IL-17C in endometriotic cells, endometrial organoids and endometriosis mice. These data defined peritoneal fluid-mediated endometriosis cancerogenesis through IL-17C regulation and suggests that IL-17C/IL-17RE can thus potentially serve as novel targets for with high IL-17C.
2025-04-30 | GSE291389 | GEO
Project description:RNA-sequencing reveals novel molecular mechanisms of endometriosis lesion development in a mouse model
| PRJNA1074834 | ENA