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Analysis of lncRNA expression in endometriosis infertility, tubal disease infertility and normal subjects

ABSTRACT: Analysis of lncRNA expression in endometriosis infertility, tubal disease infertility and normal subjects

PROVIDER: PRJNA1090075 | ENA |

REPOSITORIES: ENA

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Analysis of lncRNA expression in endometriosis infertility, tubal disease infertility and normal subjects

Project description:We found differential expression of lncRNA in the endometrium of patients with endometriosis compared to controls.

2024-03-23 | GSE262037 | GEO

Exosomal microRNAs in tubal fluid may be involved in tubal epithelial structure damage and reproductive dysfunction associated with tubal endometriosis.

Project description:Endometriosis (EM) is a well-recognized disease that causes infertility in women of reproductive age. Tubal EM adversely affects fallopian tube function and female reproductive outcomes. Our study aimed to evaluate the effect of tubal EM on tubal epithelial ultrastructure and to explore the possible mechanisms of tubal infertility by analyzing the differential expression of exosomal microRNAs (miRNAs) in tubal fluid. We obtained human fallopian tube epithelium and tubal fluid samples from patients with and without tubal EM. We used scanning electron microscopy (SEM) and transmission electron microscopy (TEM) to assess ultrastructural changes. Exosomal miRNAs in tubal fluid were extracted for microarray. We visualized epithelial damage in the tubal EM group using electron microscopy. The number of organelles decreased, and organelle structure was destroyed. A total of 14 differentially expressed exosomal miRNAs were detected in tubal fluid (fold change >2 and P value <0.05). Four miRNAs (miR-1273f, miR-5699-5p, miR-6087, miR-6747-5p) were validated by quantitative real-time polymerase chain reaction (qRT-PCR). Bioinformatic analysis showed that most of the target genes participated in embryo transport, regulation of cell communication, anatomical structure morphogenesis, and immune system processes. We verified that tubal EM damaged the tubal epithelial ultrastructure in human specimens and identified differentially expressed exosomal miRNAs in tubal liquid. These findings may elucidate the pathogenesis of tubal EM-associated infertility.

2023-06-22 | GSE220787 | GEO

Expression profiles of EMs-related infertility and tubal factor infertility granulosa cells revealed by RNA-seq

Project description:Granulosa cells are essential to the growth, development, and maturation of oocytes and follicles. In patients with EMs-related infertility, follicle maturation disorders, poor oocyte quality may be closely related to GCs in the follicle. However, the molecular biological mechanism of GCs in EMs-related infertility has not been reported. Therefore, we tried to explore the possible causes of EMs-related infertility through the study of ovarian GCs in patients with EMs-related infertility and tubal factor infertility.

2021-03-05 | GSE168214 | GEO

mRNA, lncRNA and circular RNA expression profiles and ceRNA network construction of granulosa cells in ovarian endometriosis

Project description:RNA sequencing was conducted for RNA expression profiling from GCs of five women with ovarian endometriosis and five with tubal factor infertility. The differential expression of mRNAs, lncRNAs, and circRNAs was compared. Then, the lncRNA-miRNA-mRNA and circRNA-miRNA-mRNA networks were constructed by co-expressing lncRNA/circRNA and mRNAs.

2024-12-25 | GSE192636 | GEO

Pathophysiological role of MIG-6 and ERBB2 in progesterone resistance and endometriosis-related infertility.

Project description:MIG-6 loss caused progesterone resistance through ERBB2 overexpression in non-receptive endometrium of endometriosis-related infertility. We used microarrays to understand the molecular mechanisms of progesterone resistance in infertility

2019-11-30 | GSE138185 | GEO

Exosomal microRNAs in tubal fluid may be involved in tubal epithelial structure damage and reproductive dysfunction associated with tubal endometriosis.

Project description:Exosomal microRNAs in tubal fluid may be involved in tubal epithelial structure damage and reproductive dysfunction associated with tubal endometriosis.

| PRJNA911322 | ENA

Decreased expression of EZH2 in granulosa cells contributes to endometriosis-associated infertility by targeting IL-1R2 [RNA-Seq]

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.

2025-02-28 | GSE218980 | GEO

Decreased expression of EZH2 in granulosa cells contributes to endometriosis-associated infertility by targeting IL-1R2 [ChIP-Seq]

2025-02-28 | GSE218976 | GEO

Expression profiles of EMs-related infertility and tubal factor infertility granulosa cells revealed by RNA-seq

Project description:Expression profiles of EMs-related infertility and tubal factor infertility granulosa cells revealed by RNA-seq

| PRJNA706566 | ENA

Peritoneal fluid from subjects with endometriosis regulates gene expression in cultured endometrial cells

Project description:Purpose: This study was undertaken to evaluate the effect of peritoneal fluid from subjects with differing stages of endometriosis on gene expression in endometrial stromal cells. Methods: Peritoneal fluid from subjects with minimal, moderate, and severe stages of endometriosis or without endometriosis (controls) was collected, filtered and separated from peritoneal cells. Telomerase – immortalized human endometrial stromal cells (T-HESC) were treated with the peritoneal fluid samples for 48 hours. RNA was isolated from treated cells and processed for DNA microarray. Results: 162 genes were found to be differentially expressed in T-HESC cells treated with peritoneal fluid from subjects with differing stages of endometriosis. Three of the differentially expressed genes were chosen for confirmatory studies using quantitative RT-PCR; these were interleukin 8, corin and matrix metalloproteinase 3. The primary gene ontologies identified by microarray highlight functions expected to be involved in the establishment of endometriosis, such as proteases, signal transduction, defense and immune system, cell adhesion, cell cycle and cell death, cytoskeleton, transcriptional regulation and translation, extracellular matrix, and enzymes and metabolism. Conclusions: This study demonstrated that the severity of endometriosis affected the factors present in peritoneal fluid which, in turn, affected gene expression in endometrial stromal cells.

2019-07-01 | GSE101176 | GEO

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