Nude mouse model of endometriosis
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ABSTRACT:
PROVIDER: PRJNA109079 | ENA |
REPOSITORIES: ENA
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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. Morphometric analysis of nude mouse lesions confirmed that necrosis, inflammation, healing and repair and cell proliferation occurred during xenograft development. These processes were entirely consistent with the molecular networks revealed by the microarray data. The transcripts detected in the xenografts overlapped with transcripts differentially expressed in a comparison between paired eutopic and ectopic endometrium from human endometriotic patients. For the first time components of the interaction between ectopic endometrium and peritoneal stromal tissues have been revealed in ectopic endometrial lesions. Targeted disruption of this dialogue is likely to disrupt endometriotic tissue formation and may prove to be an effective therapeutic strategy for endometriosis. Keywords: time course, disease state analysis.
2008-12-22 | GSE11768 | 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. Morphometric analysis of nude mouse lesions confirmed that necrosis, inflammation, healing and repair and cell proliferation occurred during xenograft development. These processes were entirely consistent with the molecular networks revealed by the microarray data. The transcripts detected in the xenografts overlapped with transcripts differentially expressed in a comparison between paired eutopic and ectopic endometrium from human endometriotic patients. For the first time components of the interaction between ectopic endometrium and peritoneal stromal tissues have been revealed in ectopic endometrial lesions. Targeted disruption of this dialogue is likely to disrupt endometriotic tissue formation and may prove to be an effective therapeutic strategy for endometriosis. Experiment Overall Design: Xenografts of human endometrium in nude mice hybridised to both human and mouse specific genechips. 2 biological replicates, at 3 time points. Control human endometrium and mouse pertioneum were hybridised to both human and mouse genechips
2009-01-02 | E-GEOD-11768 | biostudies-arrayexpress
Project description:Retrograde menstruation is considered a major reason for the development of endometriosis. The syngeneic transplantation mouse model is an endometriosis animal model that is considered to mimic retrograde menstruation. However, it remains poorly understood which genetic signatures of endometriosis are reflected in this model. Here, we employed an in vivo syngeneic mouse endometriosis model and identified differentially expressed genes (DEGs) between the ectopic and eutopic tissues using microarray analysis.
2022-02-28 | GSE190209 | GEO
Project description:This SuperSeries is composed of the following subset Series:; GSE11691: Euctopic and ectopic human endometrium (endometriosis); GSE11768: Nude mouse model of endometriosis Experiment Overall Design: Refer to individual Series
2009-01-02 | E-GEOD-11769 | biostudies-arrayexpress
Project description:Gene expression data from the syngeneic mouse endometriosis model
| PRJNA786343 | ENA
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: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: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:The goals of this study are to compare the different transcriptome signiture between s.c. tumors from nude mouse allografted by R728T1 (non-SMCs derived from Rb/P53 mouse model)with and without Taz knockdown with NGS-derived retinal transcriptome profiling (RNA-seq).
2019-07-22 | GSE84741 | GEO
Project description:Estrobolome dysregulation is associated with altered immunometabolism in a mouse model of endometriosis
| PRJNA1042826 | ENA