Identification of candidate microRNA biomarkers of endometriosis in different bodily fluids
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo Sapiens
SUBMITTER: 
Jinhua Leng
PROVIDER: PXD070868 | iProX | Mon Nov 17 00:00:00 GMT 2025
REPOSITORIES: iProX
Publications
Identification of candidate microRNA biomarkers of endometriosis in different bodily fluids.
Lyu Shiqing S Li Qiutong Q Gu Zhiyue Z Yan Hailan H Tang Xinyue X Dai Yi Y Li Xiaoyan X Wu Yushi Y Zhang Chenyu C Xu Yiyao Y Li Yuanyuan Y Hu Yao Y Wong Wing Hing WH Yu Yanqin Y Lu Shen S Bischoff Farideh Z FZ Leng Jinhua J Shi Jinghua J
Scientific reports 20260125 1
Endometriosis is a chronic estrogen-dependent disorder affecting up to 10% of women of reproductive age, and the absence of reliable noninvasive diagnostic tools contributes to delayed diagnosis and disease progression. To identify potential biomarkers, we profiled miRNA expression in serum, saliva, and vaginal mucus from 20 women (10 with endometriosis and 10 controls) using next-generation sequencing. Differentially expressed miRNAs were identified, and their predicted targets underwent Gene O ...[more]
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Project description:<p><strong>BACKGROUND:</strong> Endometriosis is a common benign gynaecological disorder. A number of studies have confirmed that the occurrence of disease in endometriosis patients is associated with metabolic changes in biological fluids and tissues. We set out to investigate the metabolic characteristics of follicular fluid in patients with ovarian endometriosis undergoing in vitro fertilization (IVF).</p><p><strong>METHODS:</strong> The current research project is an exploratory cohort study on endometriosis. A total of 19 infertile patients with ovarian endometriosis diagnosed by laparoscopy were enrolled in this study and 23 age- and BMI-matched controls (women with infertility due to male or tubal factors). All the patients underwent IVF treatment with a gonadotropin-releasing hormone antagonist protocol and completed follicular fluid (FF) collection at oocyte retrieval. The metabolomics of FF samples was analyzed by ultra high performance liquid chromatography-orbitrap exploris-mass spectrometer (UHPLC-OE-MS). The best combination of biomarkers was then selected by performing stepwise logistic regression analysis with backward elimination. </p><p><strong>RESULTS:</strong> Fifteen metabolites were identified as biomarkers associated with endometriosis. A final model containing 8-hydroxy-2-deoxyguanosine, biotin, n-acetyl-L-methionine and n-methylnicotinamide was constructed. Receiver operating characteristic analysis confirmed the value of these parameters in diagnosing endometriosis, with a sensitivity of 94.7% and a specificity of 95.7%. Analysis of fortification via the Kyoto Encyclopedia of Genes and Genome showed that 15 metabolites were enriched in 8 metabolic pathways.</p><p><strong>CONCLUSION:</strong> Metabolomics based on UHPLC-OE-MS effectively characterized the metabolomics analysis of FF in patients with ovarian endometriosis. These findings may provide a new basis for a better understanding of how diseases progress and for the discovery of new biomarkers. </p>
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Project description:The mechanism by which endometriosis, a common gynecological disease characterized by chronic pelvic pain and infertility, causes infertility remains elusive. Luteinized unruptured follicle syndrome, the most common type of ovulatory dysfunction, is a cause of endometriosis-associated infertility involving reduced numbers of retrieved and mature oocytes. Ovulation is controlled by luteinizing hormone and paracrine signals produced within the follicle microenvironment. Generally, interleukin (IL)-1β is elevated in endometriosis follicular fluid, whereby it amplifies ovulation signals by activating extracellular-regulated kinase 1/2 and CCAAT/enhancer binding protein β pathways. However, this amplification of ovulation by IL-1β does not occur in patients with endometriosis. To illuminate the mechanism of ovulatory dysfunction in endometriosis, we analyzed the impact of oxidative stress and IL-1β expression in endometriosis follicles. We found that oxidative stress decreased EZH2 expression and reduced H3K27Me3 levels in endometriosis ovarian granulosa cells (GCs). Selective Ezh2 depletion in mice ovarian GCs reduced fertility by disturbing cumulus-oocyte complex expansion and reducing epidermal growth factor-like factor expression. Gene expression and H3K27Me3 ChIP-sequencing of GCs revealed IL-1 receptor 2 (IL-1R2), a high-affinity IL-1β-receptor that suppresses IL-1β-mediated inflammatory cascades during ovulation, as a crucial target gene of the EZH2-H3K27Me3 axis. Moreover, IL-1β addition did not restore ovulation upon Ezh2 knockdown, indicating a vital function of IL-1R2 in endometriosis. Thus, our findings show that reducing EZH2 and H3K27Me3 in GCs suppressed ovulatory signals by increasing IL-1R2 expression, which may ultimately contribute to endometriosis-associated infertility.
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Project description:The mechanism by which endometriosis, a common gynecological disease characterized by chronic pelvic pain and infertility, causes infertility remains elusive. Luteinized unruptured follicle syndrome, the most common type of ovulatory dysfunction, is a cause of endometriosis-associated infertility involving reduced numbers of retrieved and mature oocytes. Ovulation is controlled by luteinizing hormone and paracrine signals produced within the follicle microenvironment. Generally, interleukin (IL)-1β is elevated in endometriosis follicular fluid, whereby it amplifies ovulation signals by activating extracellular-regulated kinase 1/2 and CCAAT/enhancer binding protein β pathways. However, this amplification of ovulation by IL-1β does not occur in patients with endometriosis. To illuminate the mechanism of ovulatory dysfunction in endometriosis, we analyzed the impact of oxidative stress and IL-1β expression in endometriosis follicles. We found that oxidative stress decreased EZH2 expression and reduced H3K27Me3 levels in endometriosis ovarian granulosa cells (GCs). Selective Ezh2 depletion in mice ovarian GCs reduced fertility by disturbing cumulus-oocyte complex expansion and reducing epidermal growth factor-like factor expression. Gene expression and H3K27Me3 ChIP-sequencing of GCs revealed IL-1 receptor 2 (IL-1R2), a high-affinity IL-1β-receptor that suppresses IL-1β-mediated inflammatory cascades during ovulation, as a crucial target gene of the EZH2-H3K27Me3 axis. Moreover, IL-1β addition did not restore ovulation upon Ezh2 knockdown, indicating a vital function of IL-1R2 in endometriosis. Thus, our findings show that reducing EZH2 and H3K27Me3 in GCs suppressed ovulatory signals by increasing IL-1R2 expression, which may ultimately contribute to endometriosis-associated infertility.
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Project description:Endometriosis is a common disease seen by gynecologists. Clinical features involve pelvic pain and unexplained infertility. Although endometriosis is pathologically characterized by endometrial tissue outside the normal uterine location, endometriosis is otherwise not easily explained. Endometriomas, endometriotic cysts of the ovary, typically cause pain and distortion of pelvic anatomy. To begin to understand the pathogenesis of endometriomas, we carried out transcriptome:microRNAome analysis of endometriomas and eutopic endometrium, using gene expression arrays and next generation small RNA sequencing technology. Keywords: two group comparison Patients undergoing surgery for endometriomas, suspected endometriosis, pelvic pain, abnormal uterine bleeding, pelvic organ prolapse, or uterine leiomyomas were approached for participation. After informed consent, the patients underwent scheduled surgical procedure. Tissues were collected either as cyst wall of endometrioma or endometrial curettage of hysterectomy specimen and placed directly into RNALater (Ambion, Austin, TX) and eventually frozen at -80?C. Samples were designated as endometriomas or non-endometriosis control endometrium based on surgical pathology reports. Total RNA was isolated from frozen tissue. High quality RNA was subjected to Illumina’s Human WG-6 version 2.0 BeadChips (Illumina). . *** This Series represents the transcriptome component of the study. ***
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Project description:Endometriosis is a common gynecological disorder characterized by ectopic growth of endometrium outside the uterus and associated with chronic pain and infertility. We investigated the role of LINC01133 in endometriosis, an lncRNA that has been implicated in several types of cancer. We found that LINC01133 is upregulated in ectopic endometriosis lesions. As expression appeared higher in the epithelial endometrial layer, we performed an siRNA knockdown of LINC01133 in an endometriosis epithelial cell line. Phenotypic assays indicated that LINC01133 may promote proliferation and suppress cellular migration, and affect the cytoskeleton and morphology of the cells. Gene ontology analysis of differentially expressed genes detected by RNA sequencing indicated that cell proliferation and migration pathways were affected in line with the observed phenotype. We validated upregulation of p21 and downregulation of cyclin at the protein level, which together with DNA FACS analysis indicated that the observed effects on cellular proliferation may be due to changes in cell cycle progression. Further, we validated upregulation of the protein kinase TESK1 at the protein level, and found a corresponding increased phosphorylation and therefore inactivation of the actin severing protein Cofilin, which may explain changes in the cytoskeleton and cellular migration. These results indicate that LINC01133 upregulation is associated with endometriosis, which may be due to its effects on genes involved in the cellular proliferation and migration pathways.
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Project description:Endometriosis is a common disease seen by gynecologists. Clinical features involve pelvic pain and unexplained infertility. Although endometriosis is pathologically characterized by endometrial tissue outside the normal uterine location, endometriosis is otherwise not easily explained. Endometriomas, endometriotic cysts of the ovary, typically cause pain and distortion of pelvic anatomy. To begin to understand the pathogenesis of endometriomas, we carried out transcriptome:microRNAome analysis of endometriomas and eutopic endometrium, using gene expression arrays and next generation small RNA sequencing technology. Keywords: two group comparison
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