Endometrial transcriptomic profiles in patients with severe IUA and normal control
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE224093 | GEO | 2023/06/12
REPOSITORIES: GEO
Similar Datasets
Project description:Intrauterine adhesions (IUA) are the most common reason of uterine infertility, which is characterized by partial or complete closure of uterine cavity and endometrial progressive fibrosis. This disease is often secondary to uterine curettage or other intrauterine surgery. The clinical manifestations include hypomenorrhea even amenorrhea, infertility or recurrent spontaneous abortion. In this work, endometria samples were collected from IUA and control patients. RNA-seq was performed to identify differences in circRNAs and miRNAs expression. This study may provide further insight in the mechanisms of IUA and function as preventive, predictive and therapeutic measures.
2021-06-15 | GSE165321 | 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: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:Abdominal adhesions form in response to peritoneal trauma that can occur during surgery. Postoperative adhesions, which develop in approximately 50-85% of patients who have undergone abdominal surgery, often result in severe complications, including intestinal obstruction, female infertility, chronic pain, and contraindication of surgery for future abdominal illnesses such as cancer. Here, we investigated the cell source of collagen production in postoperative adhesions and explored molecular mechanisms of adhesion using microarray.
2018-12-07 | GSE123413 | GEO
Project description:Endometrial transcriptomic profiles in patients with severe IUA and normal control
| PRJNA929647 | ENA
Project description:Following severe spinal cord injury (SCI), dysregulated neuroinflammation causes neuronal and glial apoptosis, resulting in scar and cystic cavity formation during wound healing process and ultimately atrophic nerve regrowth inhibitory microenvironment. Because of this complex and dynamic nature of SCI pathophysiology, a systemic solution for scar and cavity free wound healing while remodeling microenvironment for nerve regrowth has been rarely explored. To address this challenge, we provided a one-step solution through a self-assembly, multifunctional hydrogel depot punctually releasing the anti-inflammatory drug methylprednisolone sodium succinate (MPSS) and growth factors locally according to its pathophysiology to repair severe SCI. We found release of growth factors alone could only provide some tissues/axons protection, but failed to eliminate all cystic cavity formation. Sustained release of MPSS is sufficient to modulate dysregulated neuroinflammation and eliminate almost all cystic cavity but unable to alleviate impenetrable scar boundaries, which are largely responsive for nerve regrowth failure. Strikingly, synergically releasing anti-inflammatory drugs MPSS and growth factors in the hydrogel depot along SCI pathophysiology protected spared tissues/axons from secondary injury, promoted scar boundary and cavity free wound healing and made permissive bridges for remarkable axonal regrowth. Behavior and electrophysiology studies indicated that the remnant of spared axons but not regenerating axons mediated functional recovery, strongly suggesting that additional interventions are still required to make the rebuilt neuronal circuits perform functions. Taken together, these findings pave the way to develop a systemic solution to treat acute SCI.
2022-01-01 | GSE165635 | GEO
Project description:A label-free proteome analysis comparing changes in protein profiles of decidualized endometria and trophoblasts among women with different pregnancy outcomes, specifically a viable intrauterine pregnancy (IUP), ectopic pregnancy (EP), or early pregnancy loss (EPL), that identify potential biomarkers and provide insights into cellular pathways affected by fetus viability and location.
2021-12-16 | MSV000088572 | MassIVE
Project description:Recent studies are directed to decode the genetic signature of endometrial receptivity for better outcomes in assisted reproductive technologies. In this study, we aimed to understand the transcriptomic profile of midsecretory phase endometria of patients with recurrent pregnancy losses (RPL) and unexplained infertility (UI) by comparing with the endometria of healthy fertile women (Controls). In this prospective cohort study, we took endometrial samples from 24 patients with RPL, 24 patients with UI and 24 Controls at day 19-21 of the menstrual cycle. By performing genomic analysis, we assessed for differentially expressed genes (DEGs) and pathway analysis.
2021-01-18 | GSE165004 | GEO
Project description:Background: Preeclampsia (PE) is a placental disease characterized by hypertension and proteinuria in pregnant women, which is associated with a high maternal and infantile morbidity. However, circulating biomarkers able to predict the prognosis of PE are lacking. Methods: Thirty-eight women were included in the study. They consisted of 19 patients with PE (13 with severe PE and 6 women with non-severe PE) and 19 gestational age-matched normal pregnancy controls. We measured coagulation pathway, endothelial responses and microparticle release and circulating gene expression in PE patient groups and normotensive controls. Results: The measurement of markers associated with coagulation pathway, endothelial activation and circulating microparticles enabled to discriminate PE from normal pregnancy but were not sufficient to distinguish severe from non-severe PE. PE patients also exhibited a specific transcriptional program distinct from that of control women and subtle differences were observed between severe and non-severe PE. Functional annotation of the up-modulated signature in PE highlighted two main functions related to ribosome and complement. Importantly, we found that 8 genes were specifically up-modulated in severe preeclampsia. Among these genes, the expression of VSIG4 was significantly increased in patients with severe preeclampsia in comparison with controls and patients with non-severe preeclampsia. Conclusion: Using transcriptional signatures of blood samples, we identified the gene encoding the estrogen receptor as a potential diagnostic marker of severe preeclampsia. In addition, the determination of this gene may improve the prognostic assessment of severe preeclampsia. Thirty-eight women were included in the study: 19 patients with PE, including 6 women with non-severe PE and 13 with severe PE, and 19 women with normal pregnancy (NP) selected according to age, weight, smoking status, race, gestational age at the inclusion, and blood pH (Table 1 of manuscript). Women with NP had no history of medical illness or medication, and received routing prenatal care. The diagnostic of PE was based on a blood pressure of M-bM-^IM-% 140/90 mmHg taken twice, uricemia above normal laboratory range (120-420 M-BM-5mol/L), and proteinuria higher than 300 mg in a 24 hour-collection, occurring after 20 gestational weeks in previously normotensive women (Table 2). The criteria used to define severe PE included one of the following conditions: a blood pressure higher than 160/110 mmHg, a proteinuria higher than 1500 mg/24h), a multisystem disorder, maternal cerebral symptoms (seizures, stroke) or intrauterine growth restriction below the 3M-BM-0 percentile. Women with multiple gestations, fetal congenital malformations/chromosomal abnormalities, recent infection, antiphospholipid antibodies, trauma, drug or alcohol abuse during pregnancy, preexisting hypertension, thrombophilia with PE history, or women receiving anticoagulant or antiaggregation therapy were excluded from the study. Two microarrays (one non-severe PE and one normal) were discarded from the analysis for technical reasons. Thus, only 36 microarrays are included here.
2014-05-14 | E-GEOD-48424 | biostudies-arrayexpress
Project description:Previous publications demonstrated that there were anatomical, physiological, cellular, clinical and prognostic differences among adipose tissue present in subcutaneous areas, abdominal cavity and outside adventitial layer of artery. Thus, we wondered whether ASCs from subcutaneous adipose tissue, abdominal adipose tissue and perivascular adipose tissue were also different in gene expression. Here we performed bulk RNA-Seq assay for subcutaneous, abdominal and perivascular adipose derived stem cells.
2021-04-13 | GSE171946 | GEO