The retinol-binding protein receptor STRA6 contributes to the pathogenesis of adenomyosis via Wnt/β-catenin pathway depression [microRNA]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1011864 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25870105_1.fastq.gz | Fastqsanger.gz | |||
| SRR25870105_2.fastq.gz | Fastqsanger.gz | |||
| SRR25870106_1.fastq.gz | Fastqsanger.gz | |||
| SRR25870106_2.fastq.gz | Fastqsanger.gz | |||
| SRR25870107_1.fastq.gz | Fastqsanger.gz |
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Project description:Adenomyosis is an estrogen-dependent disease in which endometrial glands and stroma are pathologically demonstrated in the myometrium. Despite its prevalence and severity of symptoms, the precise etiology and physiopathology of adenomyosis is not well understood.Vitamin defciency increase in women with adenomyosis. Much less is known about the mechanism of their relationship. We found the retinol-binding protein receptor STRA6 upregulation in uterinespiral arteries from adenomyosis patients. The increased estrogen level promote the STRA6 expression, resulting the depressed Wnt/β-catenin signaling mediated by FASN/GSK-3β interaction. Overexpression of STRA6 induced epithelial to mesenchymal transition process. miR-1249-5p achieved its negative function by regulating the target gene through 3' UTR.The depletion of STRA6 in vivo alleviated the pathogenesis of adenomyosis. These results reveal a hitherto undesribed positive feedback loop between estrogen and STRA6 in adenomyosis pathogenesis. Components of vitamin A metabolism network have more complex activities than simply controlling or transferring VA compounds between different cells.
2023-09-06 | GSE242145 | GEO
Project description:Adenomyosis is an estrogen-dependent disease in which endometrial glands and stroma are pathologically demonstrated in the myometrium. Despite its prevalence and severity of symptoms, the precise etiology and physiopathology of adenomyosis is not well understood.Vitamin defciency increase in women with adenomyosis. Much less is known about the mechanism of their relationship. We found the retinol-binding protein receptor STRA6 upregulation in uterinespiral arteries from adenomyosis patients. The increased estrogen level promote the STRA6 expression, resulting the depressed Wnt/β-catenin signaling mediated by FASN/GSK-3β interaction. Overexpression of STRA6 induced epithelial to mesenchymal transition process. miR-1249-5p achieved its negative function by regulating the target gene through 3' UTR.The depletion of STRA6 in vivo alleviated the pathogenesis of adenomyosis. These results reveal a hitherto undesribed positive feedback loop between estrogen and STRA6 in adenomyosis pathogenesis. Components of vitamin A metabolism network have more complex activities than simply controlling or transferring VA compounds between different cells.
2023-09-06 | GSE242148 | GEO
Project description:The retinol-binding protein receptor STRA6 contributes to the pathogenesis of adenomyosis via Wnt/β-catenin pathway depression
| PRJNA1011857 | ENA
Project description:The retinol-binding protein receptor STRA6 contributes to the pathogenesis of adenomyosis via Wnt/β-catenin pathway depression [RNA]
| PRJNA1011862 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-09-06 | GSE242149 | GEO
Project description:Adenomyosis is defined by the presence of endometrial glands and stroma within the myometrium. Despite its frequent occurrence, the precise aetiology and physiopathology of adenomyosis is still unknown. WNT/?-catenin signalling molecules are important and should be tightly regulated for uterine function. To investigate the role of ?-catenin signalling in adenomyosis, the expression of ?-catenin was examined. Nuclear and cytoplasmic ?-catenin expression was significantly higher in epithelial cells of human adenomyosis compared to control endometrium. To determine whether constitutive activation of ?-catenin in the murine uterus leads to development of adenomyosis, mice that expressed a dominant stabilized ?-catenin in the uterus were used by crossing PR-Cre mice with Ctnnb1(f(ex3)/+) mice. Uteri of PR(cre) (/+) Ctnnb1(f(ex3)/+) mice displayed an abnormal irregular structure and highly active proliferation in the myometrium, and subsequently developed adenomyosis. Interestingly, the expression of E-cadherin was repressed in epithelial cells of PR(cre) (/+) Ctnnb1(f(ex3)/+) mice compared to control mice. Repression of E-cadherin is one of the hallmarks of epithelial-mesenchymal transition (EMT). The expression of SNAIL and ZEB1 was observed in some epithelial cells of the uterus in PR(cre) (/+) Ctnnb1(f(ex3)/+) mice but not in control mice. Vimentin and COUP-TFII, mesenchymal cell markers, were expressed in some epithelial cells of PR(cre) (/+) Ctnnb1(f(ex3)/+) mice. In human adenomyosis, the expression of E-cadherin was decreased in epithelial cells compared to control endometrium, while CD10, an endometrial stromal marker, was expressed in some epithelial cells of human adenomyosis. These results suggest that abnormal activation of ?-catenin contributes to adenomyosis development through the induction of EMT.
| S-EPMC4105844 | biostudies-literature
Project description:Aberrant activation of TGF-β2 plays an important role in the pathogenesis of adenomyosis. We used microarrays to detail the machanism underlying aberrant activation of TGF-β2 in adenomyosis
2016-10-19 | GSE88911 | GEO
Project description:Adenomyosis mostly occurs in the females with reproductive age, and the pathogenesis is not clear. If we want to improve the diagnosis and treatment of adenomyosis, we must fully understand the specific molecular mechanism of adenomyosis. The Arraystar Human m6a-mRNA&lncRNA Epitranscriptomic microarray analysis was performed on endometrial specimens of 3 patients in the human adenomyosis group and 3 patients in the normal control group to compare and screen the m6A marker of adenomyosis, providing reference for clinical treatment.
2022-10-06 | GSE214850 | GEO
Project description:Abstract: Objective: Adenomyosis is a clinical disorder defined by the presence of endometrial glands and stroma within the myometrium, the pathogenesis of which is poorly understood. We postulate that dysregulation of genes and pathways in eutopic endometrium may predispose to ectopic implantation. No study, to our knowledge, has examined the global transcriptome of isolated eutopic endometrium from women with clinically significant adenomyosis. Design: Laboratory-based study with full IRB approval and consents. Material and Methods: Endometrial sampling was performed on hysterectomy specimens (proliferative phase) from symptomatic women with pathologically-confirmed diffuse adenomyosis (n=3). Controls (n=5) were normo-ovulatory subjects without adenomyosis. All subjects were free from leiomyoma, endometriosis, and hormonal exposures. Isolated purified total RNA was subjected to microarray analysis using the Gene 1.0 ST Affymetrix platform. Data were analyzed with GeneSpring and Ingenuity Pathway analysis. Validation of several genes was undertaken by QRT-PCR. Results: Comparison of transcriptomes of proliferative endometrium from women with and without adenomyosis revealed 140 up-regulated and 884 down-regulated genes in samples from women with adenomyosis compared to controls. Highly differentially expressed genes include those involved in regulation of apoptopsis, steroid hormone responsiveness, and proteins involved in extracellular matrix remodeling, as well as microRNAs of unknown significance. Affected canonical pathways included eukaryotic initiation factor 2 signaling, oxidative phosphorylation, mitochondrial dysfunction, estrogen receptor signaling, and mTOR signaling. Conclusions: The eutopic endometrium in patients with adenomyosis has fundamental abnormalities that may predispose to invasion and survival beyond the myometrial interface. Key Words: adenomyosis, endometrium, microarray, microRNA, endometriosis, apoptosis, signaling. Abstract: Objective: Adenomyosis is a clinical disorder defined by the presence of endometrial glands and stroma within the myometrium, the pathogenesis of which is poorly understood. We postulate that dysregulation of genes and pathways in eutopic endometrium may predispose to ectopic implantation. No study, to our knowledge, has examined the global transcriptome of isolated eutopic endometrium from women with clinically significant adenomyosis. Design: Laboratory-based study with full IRB approval and consents. Material and Methods: Endometrial sampling was performed on hysterectomy specimens (proliferative phase) from symptomatic women with pathologically-confirmed diffuse adenomyosis (n=3). Controls (n=5) were normo-ovulatory subjects without adenomyosis. All subjects were free from leiomyoma, endometriosis, and hormonal exposures. Isolated purified total RNA was subjected to microarray analysis using the Gene 1.0 ST Affymetrix platform. Data were analyzed with GeneSpring and Ingenuity Pathway analysis. Validation of several genes was undertaken by QRT-PCR. Results: Comparison of transcriptomes of proliferative endometrium from women with and without adenomyosis revealed 140 up-regulated and 884 down-regulated genes in samples from women with adenomyosis compared to controls. Highly differentially expressed genes include those involved in regulation of apoptopsis, steroid hormone responsiveness, and proteins involved in extracellular matrix remodeling, as well as microRNAs of unknown significance. Affected canonical pathways included eukaryotic initiation factor 2 signaling, oxidative phosphorylation, mitochondrial dysfunction, estrogen receptor signaling, and mTOR signaling. Conclusions: The eutopic endometrium in patients with adenomyosis has fundamental abnormalities that may predispose to invasion and survival beyond the myometrial interface. Key Words: adenomyosis, endometrium, microarray, microRNA, endometriosis, apoptosis, signaling. A total of 8 samples were used and analyzed by disease state. Endometrial samples from hysterectomy specimens in proliferative phase of menstrual cycle from symptomatic women with pathologically-confirmed diffuse adenomyosis were compared with endometrial samples from normo-ovulatory healthy subjects with no endometrial or uterine pathology.
2016-03-03 | E-GEOD-78851 | biostudies-arrayexpress
Project description:Diabetic cardiomyopathy (DCM) is a primary myocardial injury induced by diabetes mellitus (DM) with a complex pathogenesis. In this study, we identified disordered cardiac retinol metabolism in T2DM mice and patients characterized by retinol (vitamin A, Rol) overload, all-trans retinoic acid (atRA) deficiency and retinoic acid receptors (RARs) reduction, and demonstrated that both cardiac Rol overload and atRA deficiency promote DCM by supplementing T2DM mice with Rol or atRA. Mechanically, by constructing cardiomyocyte-specific conditional RDH10-knockout mice and overexpressing RDH10 in T2DM mice via adeno-associated virus, we verified that the reduction in cardiac retinol dehydrogenase 10 (RDH10) is the initiating factor for cardiac retinol metabolism disorder and its resulting DCM. Additionally, lipotoxicity and ferroptosis contribute to the effect of retinol metabolism disorder on DCM. Based on these results, we suggest that the reduction of cardiac RDH10 and its mediated disorder of cardiac retinol metabolism is a new mechanism underlying DCM.
2023-01-15 | GSE202418 | GEO