Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA251513 | ENA |
REPOSITORIES: ENA
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Project description:Endometriosis is an estrogen-dependent inflammatory disease. A pivotal contributor to endometriosis is the estrogen receptor beta (ERβ), which drives the condition by impeding cell death through interferon (IFN) signaling. One noteworthy component of this cascade is the N-myc and STAT Interactor (NMI), an interferon alpha (IFNα) target gene whose expression is repressed in endometriotic lesions compared to normal endometrium. This repression is particularly pronounced in stromal cells, mediated by ERβ. The results of Western blot analyses, comparing IFNα-treated and untreated cells, demonstrate that IFNα treatment triggers cell death signaling, including apoptosis and necroptosis, in endometrial stromal cells. Intriguingly, NMI knockdown (KD) obstructed IFNα-induced cell death signaling in human endometrial stromal cells. Moreover, NMI KD amplified non-canonical IFNα pathways, such as β-Catenin/GSK3β and PI3K/AKT signaling, in endometrial stromal cells following IFNα treatment. RNA sequencing analyses unveiled that NMI KD augmented the expression of genes responsible for cell-cell adhesion and extracellular structural organization in IFNα-independent manners. These findings suggest that NMI KD plays an indispensable role in enhancing the adhesion and invasion of endometriotic cells during endometriosis progression. In summary, NMI functions as an endometriosis suppressor gene in endometriotic stromal cells, curbing the advancement of endometriosis. This intricate interplay of ERβ, IFNα signaling, and NMI offers novel insights into the mechanisms governing endometriosis development.
2025-08-31 | GSE241751 | GEO
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
Project description:Background Reduced endometrial receptivity is a major factor for impaired fertility in endometriosis (EMS). Endometrial deposition of collagen I proteins may account for poor endometrial receptivity in endometriosis. Methods We investigated the expression of collagen I expression in endometrium of endometriosis patients and in constructed EMS mice model. Effect of collagen I on ESCs was evaluated. Co-culture of exosomes with ESCs was conducted to evaluate the uptake of exosomes by different endometrial cell lines and the effect on decidualization of eutopic ESCs and embryo implantation. MiRNA expression profiles were compared between ectopic ESC derived exosomes and eutopic ESC derived exosomes. Luciferase reporter and its mutant plasmids were applied to confirm the direct target of miR-25-3p. Findings Here we found endometrial collagen I deposition with impaired decidualization in endometriosis patients and EMS mice model. Treatment of collagen I with ESCs contributed to impaired decidualization and inhibited BLS expansion in vitro. Endometriotic stromal cell-derived exosomes were detected in eutopic endometrium and the ectopic endometrial stromal cell derived exosomes were more taken-up by the same cell line in eutopic endometrium. Treatment of endometriotic stromal cell-derived exosomes increased the expression of endometrial collagen I in vitro and in vivo, while inhibited BLS expansion. Exosomal miR-25-3p was significantly increased in endometriotic stromal cell-derived exosomes compared with control group, and PTEN is a certain target of miR-25-3p. The promotion of endometrial miR-25-3p significantly increased collagen I expression in vitro through the PTEN/Akt pathway. Interpretation These results suggested that endometriotic stromal cell-derived exosomal miR-25-3p played key role in inducing endometrial collagen I deposition to impair embryo expansion in endometriosis via PTEN/Akt pathway. Funding National Nature Science Foundation of China (82271702), National Natural Science Foundation of China (81771537). Keywords: endometriosis; exosome; collagen I; miRNA; collagen deposition
2025-01-28 | GSE222432 | GEO
Project description:Compulsory expression of miR-210 in normal endometrial stromal cells directed the induction of cell proliferation and vascular endothelial growth factor production, and the inhibition of apoptosis in through signal transducer and activator of transcription 3 (STAT3) activation. Accumulating evidence suggests that microRNAs play definite roles in the pathogenesis of endometriosis. The objective of the study was to determine the role of miR-210, one of the upregulated microRNA in endometriotic cyst stromal cells, in the pathogenesis of endometriosis. Downstream targets of miR-210 were identified by Compulsory expression of miR-210 in normal eutopic endometrial stromal cells, a global mRNA microarray technique, and Ingenuity pathways analysis.
2015-04-06 | GSE56854 | GEO
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.
2016-10-22 | MSV000080276 | MassIVE
Project description:We utilized fluorescence-activated cell sorting to isolate endometrial stromal cells from paired endometrial and endometrioma biopsies and combined it with high-throughput sequencing to determine miRNA alterations in endometriotic stroma. The analysis revealed 149 abnormally expressed miRNAs in endometriotic lesions, including extensive upregulation of miR-139-5p and downregulation of miR-375 compared to eutopic cells. The results of this study provide further insights into the complex molecular mechanisms involved in endometriosis pathogenesis and demonstrate the necessity for cell-type specific analysis of ectopic tissues to understand the interactions between different cell populations in disease onset and progression.
2019-01-15 | GSE121406 | GEO
Project description:Endometriosis is an inflammatory disease and bone marrow-derived cells are abundant in endometriotic lesions and in the peritoneal fluid of women with the disease. This study tested the hypothesis that reciprocal communication occurs between macrophages and cultured human endometrial stromal cells and that this communication contributes to the pathology of endometriosis. Changes in gene expression elicited by exposure to factors secreted by the opposing cell type were measured by DNA microarray to test this hypothesis. 716 named genes were differentially expressed in cultured endometrial stromal cells in response to factors secreted by macrophages. Genes that were up-regulated included IL8/CXCL8, MMP3, phospholamban, CYR61/CCN1, CTGF/CCN2, tenascin C, and NNMT, whereas integrin alpha 6 was down-regulated. In contrast, 15 named genes were differentially expressed in macrophages in response to factors secreted by cultured endometrial stromal cells. The data document reciprocal communication between macrophages and endometrial stromal cells and suggest that interaction with macrophages stimulates the expression of genes in endometrial stromal cells that contribute to migration, adhesion, invasion, neovascularization and mitosis of endometrial cells that may support the establishment of endometriosis.
2010-07-21 | GSE19834 | GEO
Project description:Accumulating evidence suggests that microRNAs play definite roles in the pathogenesis of endometriosis. The objective of the study was to determine the role of miR-100-5p, one of the upregulated microRNA in endometriotic cyst stromal cells, in the pathogenesis of endometriosis. Downstream targets of miR-100-5p were identified by compulsory expression of miR-100-5p in normal eutopic endometrial stromal cells (NESCs), a global mRNA microarray technique, and pathways analysis.Compulsory expression of miR-100-5p in NESCs directed the induction of cell motility through SWItch/sucrose non-fermentable (SWI/SNF)-related matrix-associated actin-dependent regulator of chromatin subfamily D member 1 (SMARCD1) supression and matrix metallopeptidase 1 (MMP1) activation.
2020-04-22 | GSE139954 | GEO
Project description:Compulsory expression of miR-210 in normal endometrial stromal cells directed the induction of cell proliferation and vascular endothelial growth factor production, and the inhibition of apoptosis in through signal transducer and activator of transcription 3 (STAT3) activation. Accumulating evidence suggests that microRNAs play definite roles in the pathogenesis of endometriosis. The objective of the study was to determine the role of miR-210, one of the upregulated microRNA in endometriotic cyst stromal cells, in the pathogenesis of endometriosis. Downstream targets of miR-210 were identified by Compulsory expression of miR-210 in normal eutopic endometrial stromal cells, a global mRNA microarray technique, and Ingenuity pathways analysis. NESCs were transfected with precursor hsa-miR-210 (Pre-miRTM miRNA precursor- hsa-miR-210, Ambion, Austin, TX, USA) or negative control precursor miRNA (Pre-miRTM miRNA precursor-negative control #1 Ambion) at a final concentration of 10 nM, using LipofectamineTM RNAiMAX (Invitrogen, Carlsbad, CA, USA). Forty-eight hours after transfection, total RNA from cultured NESCs transfected with precursor hsa-miR-210 (n=4) and NESCs (n=4) transfected with negative control precursor miRNA was extracted with an RNeasy Mini kit (Qiagen, Valencia, CA, USA). Then, the samples were subjected to a gene expression microarray analysis with a commercially available human mRNA microarray (G4845A, Human Gene Expression 4x44K v2, Agilent Technologies, Santa Clara, CA, USA).
2015-04-06 | E-GEOD-56854 | biostudies-arrayexpress
Project description:In this study, we characterize the fusion protein produced by the EPC1-PHF1 translocation in Low Grade Endometrial Stromal Sarcoma (LG-ESS) and Ossifying FibroMyxoid Tumors (OFMT). We express the fusion protein and necessary controls in K562 Cells. The fusion protein assembles a mega-complex harboring both NuA4/TIP60 and PRC2 subunits and enzymatic activities and leads to mislocalization of chromatin marks in the genome, linked to aberrant gene expression.
2020-11-25 | GSE162118 | GEO