Genome-wide analysis of human endometria
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE165321 | GEO | 2021/06/15
REPOSITORIES: GEO
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Project description:Intrauterine adhesion (IUA) is characterized by endometrial fibrosis with partial or complete uterine cavity obliteration. IUA patients often undergo amenorrhea/ hypomenorrhea, abdominal pain, infertility, early pregnancy loss or severe placental complications. In this work, endometria samples were collected from severe IUA and control patients. RNA-seq was performed to identify differences between IUA and normal control and investigate the mechanisms of IUA development.
2023-06-12 | GSE224093 | GEO
Project description:Intrauterine adhesion (IUA), characterized by endometrial fibrosis, is a common cause of female reproductive disorders. IUA-like mice model was created with curettage plus LPS stimulation to mimic endometrial fibrosis in IUA patients. Mesenchymal stem cells (MSCs) based therapy is applied to some refractory immune diseases to control inflammation and their immunomodulatory function can be enhanced via pre-treatment with inflammatory cytokines. In this work, we examined the effect of untreated and cytokines primed MSCs therapy on macrophage in IUA-like mice model. The uteri samples were collected from sham, IUA modeling, IUA+control MSCs treatment and IUA+primed MSCs treatment groups of mice. Endometrial macrophages were sorted through F4/80 magnetic beads and performed RNA-seq.
2023-06-12 | GSE224288 | GEO
Project description:Background: Abnormal autophagy and TGFβ-SMAD3/7 signaling pathway plays an important role in intrauterine adhesions (IUA); however, the exact underlying mechanisms remain unclear. In this study, we aimed to detect whether SMAD7 effected IUA via regulating autophagy and TGFβ-SMAD3 signaling pathway. Methods: The expression of p-SMAD3 and SMAD7 were detected by Immunohistochemistry. Endometrial fibrosis was detected by masson staining. The expression of protein related to autophagy and fibrosis was detected by western blot. The autophagic flux was monitored via Tandem mRFP-GFP-LC3 fluorescence system. Chip assay was used for SMAD3 binding site analysis. SMAD7 knockout mice were used to investigate the regulation of SMAD7 on intrauterine adhesions and autophagy. Results: we observed that patients with IUA exhibited a lower expression of SMAD7. In endometrial stromal cells, the silencing of SMAD7 inhibited autophagic flux, whereas overexpressed SMAD7 promoted autophagic flux. We also found that SMAD7-mediated autophagic flux regulated stromal-myofibroblast transition. These phenotypes are regulated by the transforming growth factor (TGF)β-SMAD3 signaling pathway. We found that SMAD3 directly binds to the 3ʹ-untranslated region of transcription factor EB (TFEB) and inhibits its transcription. SMAD7 promoted autophagic flux by inhibiting SMAD3, thereby promoting the expression of TFEB. The endometria of SMAD7 knockout mice showed a fibrotic phenotype. Simultaneously, autophagic flux was inhibited. On administering the autophagy activator rapamycin, endometrial fibrosis of SMAD7 gene conditional knockout mice was partially restored. Conclusions: The loss of SMAD7 promotes endometrial fibrosis by inhibited autophagic flux via the TGFβ-SMAD3 pathway. Therefore, this study reveals a potential therapeutic target for IUA.
2024-10-11 | GSE272824 | GEO
Project description:Transcriptome sequencing of uterine scar tissue in patients with intrauterine adhesions
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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. ***
2011-05-09 | E-GEOD-23339 | biostudies-arrayexpress
Project description:Purpose: The fundamental cause of intrauterine adhesions (IUAs) is the destruction and reduction of stem cells in endometrial basal layer, resulting in endometrial reconstruction very difficult. The purpose of this study was to investigate the effects and underlying mechanism of human umbilical cord blood derived mesenchymal stem cells (hUCB-MSC) on the endometrial reconstruction after transplantation. Methods: hUCB-MSCs were isolated and identified successfully. The rabbit IUA models were established and set five groups (control, 14/28th day after surgery, estrogen and hUCB-MSCs treatment).The number of endometrial glands and the fibrosis rate were evaluated using HE and Masson staining, respectively. Endometrial proliferation, angiogenesis and inflammation was evaluated by immunohistochemical staining of ER, Ki-67and TGF-β1, respectively. Single-cell RNA sequencing (scRNA-seq) was applied to explore the cell differentiation trajectory after hUCB-MSCs transplanted into IUA endometrium. Finally, molecular mechanism of hUCB-MSCs repairing damaged endometrium was investigated by RNA sequencing. Results: After transplantation of the hUCB-MSCs, the increase of endometrial gland number, estrogen receptor(ER) and Ki-67expression,and the decrease of fibrosis rate and TGF-β expression(P＜0.05), suggested the endometrial repair, angiogenesis and inflammatory suppression. The therapeutic effect of hUCB-MSCs was significantly improved compared with 28th day after surgery and estrogen group. ScRNA-seq demonstrated that the transplanted hUCB-MSCs can trans-differentiate into endometrial cells: epithelial, fibroblast, and macrophage. RNA Sequencing of six IUA samples further revealed that hUCB-MSCs may regulate Th17/Treg balance through NF-B signaling, thus inhibiting the immune response of damaged endometrium. Conclusions: Our study demonstrated that hUCB-MSCs can repair damaged endometrium through trans-differentiation, immunomodulatory capacities, and NF-κB signaling, suggesting the treatment value of hUCB-MSCs in IUA.
2022-06-21 | GSE205996 | GEO
Project description:Purpose: The fundamental cause of intrauterine adhesions (IUAs) is the destruction and reduction of stem cells in endometrial basal layer, resulting in endometrial reconstruction very difficult. The purpose of this study was to investigate the effects and underlying mechanism of human umbilical cord blood derived mesenchymal stem cells (hUCB-MSC) on the endometrial reconstruction after transplantation. Methods: hUCB-MSCs were isolated and identified successfully. The rabbit IUA models were established and set five groups (control, 14/28th day after surgery, estrogen and hUCB-MSCs treatment).The number of endometrial glands and the fibrosis rate were evaluated using HE and Masson staining, respectively. Endometrial proliferation, angiogenesis and inflammation was evaluated by immunohistochemical staining of ER, Ki-67and TGF-β1, respectively. Single-cell RNA sequencing (scRNA-seq) was applied to explore the cell differentiation trajectory after hUCB-MSCs transplanted into IUA endometrium. Finally, molecular mechanism of hUCB-MSCs repairing damaged endometrium was investigated by RNA sequencing. Results: After transplantation of the hUCB-MSCs, the increase of endometrial gland number, estrogen receptor(ER) and Ki-67expression,and the decrease of fibrosis rate and TGF-β expression(P＜0.05), suggested the endometrial repair, angiogenesis and inflammatory suppression. The therapeutic effect of hUCB-MSCs was significantly improved compared with 28th day after surgery and estrogen group. ScRNA-seq demonstrated that the transplanted hUCB-MSCs can trans-differentiate into endometrial cells: epithelial, fibroblast, and macrophage. RNA Sequencing of six IUA samples further revealed that hUCB-MSCs may regulate Th17/Treg balance through NF-B signaling, thus inhibiting the immune response of damaged endometrium. Conclusions: Our study demonstrated that hUCB-MSCs can repair damaged endometrium through trans-differentiation, immunomodulatory capacities, and NF-κB signaling, suggesting the treatment value of hUCB-MSCs in IUA.
2022-06-21 | GSE205992 | GEO
Project description:Asherman’s Syndrome is characterized by intrauterine adhesions or scarring, which cause infertility, menstrual abnormalities, and recurrent pregnancy loss. The pathophysiology of this syndrome remains unknown, with treatment restricted to recurrent surgical removal of intrauterine scarring, which has limited success. Here, we decode the Asherman’s Syndrome endometrial cell niche by analyzing data from over 200,000 cells with single-cell RNA-sequencing in patients with this condition and through in vitro analyses of Asherman’s Syndrome patient-derived endometrial organoids. Our endometrial atlas highlights the loss of the endometrial epithelium, alterations to epithelial differentiation signaling pathways such as Wnt and Notch, and the appearance of characteristic epithelium expressing secretory leukocyte protease inhibitor during the window of implantation. We describe syndrome-associated alterations in cell-to-cell communication and gene expression profiles that support a dysfunctional pro-fibrotic, pro-inflammatory, and anti-angiogenic environment.
2023-08-03 | GSE216748 | GEO
Project description:Asherman’s Syndrome is characterized by intrauterine adhesions or scarring, which cause infertility, menstrual abnormalities, and recurrent pregnancy loss. The pathophysiology of this syndrome remains unknown, with treatment restricted to recurrent surgical removal of intrauterine scarring, which has limited success. Here, we decode the Asherman’s Syndrome endometrial cell niche by analyzing data from over 200,000 cells with single-cell RNA-sequencing in patients with this condition and through in vitro analyses of Asherman’s Syndrome patient-derived endometrial organoids. Our endometrial atlas highlights the loss of the endometrial epithelium, alterations to epithelial differentiation signaling pathways such as Wnt and Notch, and the appearance of characteristic epithelium expressing secretory leukocyte protease inhibitor during the window of implantation. We describe syndrome-associated alterations in cell-to-cell communication and gene expression profiles that support a dysfunctional pro-fibrotic, pro-inflammatory, and anti-angiogenic environment.
2023-08-03 | GSE215968 | GEO
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