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.
Project description:The hypothesis that male michrochimerism in eutopic endometrium is a factor for endometriosis, as indicated by indirect evidence was examined in endometrial samples from control (Group 1) and stage IV ovarian endometriosis (Group 2), either fertile (Group 1A and 2A) or Infertile (Group 1B and 2B) pateints. 6 coding and 10 non-coding genes showed bi-modal pattern of expression characterised by low expression in samples obtained from fertile patients and high expressions in infertile patients. Several coding and non-coding MSY-linked genes displayed michrochimerism in form of presence of their respective DNA inserts along with their microarray-detectable expression in endometrium irrespective of fertility history and disease.
Project description:Analysis of endometriosis disease associated tissues, endometrium and peritoneum at gene expression level. In this study we present, an interactive web-based user interface for browsing gene expression patterns in the normal endometrium, peritoneum and endometriotic lesions. This tool allows users to explore gene expression profiles of genes of interests in the endometrium and different lesion types without the requirement of advanced computational skills.
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
Project description:This project aims at comparing endometrium from women with and without endometriosis during the secretory phase of menstrual cycle. The present results constitute a first step towards identifying potential diagnosis biomarkers and may provide a better understanding of endometriosis especially the etiology of the disease.
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)
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)
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.