Duodenal Mucosal Barrier in Functional Dyspepsia [mRNA]
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ABSTRACT:
PROVIDER: PRJNA716245 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14028840_1.fastq.gz | Fastqsanger.gz | |||
| SRR14028840_2.fastq.gz | Fastqsanger.gz | |||
| SRR14028841_1.fastq.gz | Fastqsanger.gz | |||
| SRR14028841_2.fastq.gz | Fastqsanger.gz | |||
| SRR14028842_1.fastq.gz | Fastqsanger.gz |
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Project description:Epithelial Barrier and Leaky Gut in Dyspepsia Running title: Epithelial Barrier and Leaky Gut in Dyspepsia Context: Some studies suggest that FD is associated with ex vivo duodenal epithelial micro-inflammation and barrier impairment; the pathogenesis of these findings is unclear. miRNAs reduce expression of epithelial barrier genes and have been postulated to increase epithelial permeability in irritable bowel syndrome. New findings: Compared to controls, there is reduced mRNA expression of several barrier proteins (zona occludin-1), increased expression of several miRNAs (eg, miR-142-3p) that suppress the genes for barrier proteins in FD. However, mucosal eosinophils, intraepithelial lymphocytes, and mast cells, ex- and in vivo permeability (urinary lactulose and mannitol excretion) were not significantly different in FD. Impact: Patients with FD do not have a leaky gut syndrome.
2023-03-01 | GSE169304 | GEO
Project description:Duodenal Mucosal Barrier in Functional Dyspepsia
| PRJNA716241 | ENA
Project description:Epithelial Barrier and Leaky Gut in Dyspepsia Running title: Epithelial Barrier and Leaky Gut in Dyspepsia Context: Some studies suggest that FD is associated with ex vivo duodenal epithelial micro-inflammation and barrier impairment; the pathogenesis of these findings is unclear. miRNAs reduce expression of epithelial barrier genes and have been postulated to increase epithelial permeability in irritable bowel syndrome. New findings: Compared to controls, there is reduced mRNA expression of several barrier proteins (zona occludin-1), increased expression of several miRNAs (eg, miR-142-3p) that suppress the genes for barrier proteins in FD. However, mucosal eosinophils, intraepithelial lymphocytes, and mast cells, ex- and in vivo permeability (urinary lactulose and mannitol excretion) were not significantly different in FD. Impact: Patients with FD do not have a leaky gut syndrome.
2023-03-01 | GSE169307 | GEO
Project description:Duodenal Mucosal Barrier in Functional Dyspepsia [miRNA]
| PRJNA716246 | ENA
Project description:Background & aimsIn addition to gastric sensorimotor dysfunctions, functional dyspepsia (FD) is also variably associated with duodenal micro-inflammation and epithelial barrier dysfunction, the pathogenesis and clinical significance of which are unknown. Our hypothesis was that miRNAs and/or inflammation degrade epithelial barrier proteins, resulting in increased duodenal mucosal permeability in FD.MethodsWe compared the duodenal mucosal gene expression and miRNAs, in vivo permeability (lactulose-mannitol excretion between 0 and 60 and 60 and 120 minutes after saccharide ingestion), ex vivo assessments (transmucosal resistance, fluorescein isothiocyanate [FITC]-dextran flux, and basal ion transport), and duodenal histology (light and electron microscopy) in 40 patients with FD and 24 controls.ResultsCompared with controls, the mRNA expression of several barrier proteins (zonula occludens-1, occludin, claudin-12, and E-cadherin) was modestly reduced (ie, a fold change of 0.8-0.85) in FD with increased expression of several miRNAs (eg, miR-142-3p and miR-144-3-p), which suppress these genes. The urinary lactulose excretion and the lactulose:mannitol ratio between 60 and 120 minutes were greater in FD than in controls (P < .05). The FITC-dextran flux, which reflects paracellular permeability, was inversely correlated (r = -0.32, P = .03) with transmucosal resistance and directly correlated (r = 0.4, P = .02) with lactulose:mannitol ratio. Other parameters (mucosal eosinophils, intraepithelial lymphocytes, and mast cells, transmucosal resistance, FITC-dextran flux, average intercellular distance, and proportion of dilated junctions) were not significantly different between groups.ConclusionsIn FD, there is a modest reduction in the expression of several duodenal epithelial barrier proteins, which may be secondary to up-regulation of regulatory miRNAs, and increased small intestinal permeability measured in vivo.
| S-EPMC8975906 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-03-01 | GSE169308 | GEO
Project description:Gene expression was detected using duodenal samples to identify the key regulatory genes for the treatment of dyspepsia with Jianwei Xiaoshi oral liquid
2023-12-31 | GSE245835 | GEO
Project description:ObjectivesThe pathophysiology of functional dyspepsia (FD) is not fully understood. Impaired duodenal mucosal integrity characterized by increased mucosal permeability and/or low-grade inflammation was reported as potentially important etiologies. We aimed to determine the utility of a recently developed simple catheterization method to measure mucosal admittance (MA), the inverse of mucosal impedance, for evaluation of duodenal mucosal permeability in patients with FD.MethodsWe conducted two prospective studies. In the first study, duodenal MA of 23 subjects was determined by catheterization during upper endoscopy, and transepithelial electrical resistance (TEER) of duodenal biopsy samples in Ussing chambers was measured to assess the correlation between MA and TEER. In the second study, duodenal MA of 21 patients with FD fulfilling the Rome III criteria was compared with that of 23 healthy subjects.ResultsThe mean MA and TEER values were 367.5±134.7 and 24.5±3.7 Ω cm2, respectively. There was a significant negative correlation between MA and TEER (r=-0.67, P=0.0004, Pearson's correlation coefficient). The mean MA in patients with FD was significantly higher than that in healthy subjects (455.7±137.3 vs. 352.1±66.9, P=0.002, unpaired t-test). No procedure-related complications were present.ConclusionsWe demonstrated the presence of increased duodenal mucosal permeability in patients with FD by MA measurement using a simple catheterization method during upper endoscopy.
| S-EPMC5415894 | biostudies-literature
Project description:Proteomic analysis was conducted on gastric and duodenal tissues from rats with functional dyspepsia of spleen deficiency and normal rats, as well as rats with functional dyspepsia treated with Jianwei Xiaoshi tablets.
2023-11-29 | PXD047366 |
Project description:Introduction. Hindered by a limited understanding of the molecular mechanisms responsible for diabetic gastroenteropathy (DGE), patients are managed by symptom-based therapies. We investigated the duodenal mucosal expression of protein-coding genes and miRNAs in DGE and related these abnormalities to clinical features. Methods. mRNA and micro RNA (miRNA) expression and ultrastructure of duodenal mucosal biopsies were investigated in 39 DGE patients and 21 healthy controls. Results were analyzed in the context of diabetic phenotype and gastric emptying. Results. There were 3175 differentially-expressed genes (FDR<0.05), especially mitochondrial genes, in DGE versus controls. Several mitochondrial (mt) DNA-encoded genes (12 of 13 protein coding genes mainly involved in oxidative phosphorylation (OXPHOS), both rRNAs and 9 of 22 tRNAs) were downregulated; conversely, nuclear (n) DNA-encoded mitochondrial genes (eg, OXPHOS, TCA cycle) were upregulated in DGE. Motif analysis uncovered binding sites for transcription factors NRF1, GABPA and YY1, which regulate mitochondrial biogenesis, in the promoters of differentially expressed genes. Seventeen of 30 differentially expressed miRNAs in DGE targeted differentially expressed mitochondrial genes. Mitochondrial density was also reduced and correlated with the expression of 9 mt-DNA OXPHOS genes in DGE. Uncovered by a principal component (PC) analysis of OXPHOS genes, PC1 was significantly associated with neuropathy (P = 0.01) and with delayed gastric emptying (P < 0.05). Conclusion. In DGE, mtDNA- and nDNA-encoded mitochondrial genes are reduced and increased, respectively, associated with reduced mitochondrial density, neuropathy, and delayed gastric emptying, and correlated with cognate miRNA expression. Together, these findings provide substantial evidence for clinically-relevant mitochondrial disturbances in DGE.
2021-03-10 | GSE151495 | GEO