Chronic gastritis.
Ontology highlight
ABSTRACT:
SUBMITTER: Sipponen P
PROVIDER: S-EPMC4673514 | biostudies-other | 2015 Jun
REPOSITORIES: biostudies-other
Similar Datasets
Project description:Chronic atrophic gastritis (CAG) is a very common gastritis and one of the major precursor lesions of gastric cancer, one of the most common cancers worldwide. The molecular mechanism underlying CAG is unclear, but its elucidation is essential for the prevention and early detection of gastric cancer and appropriate intervention. A combination of two-dimensional gel electrophoresis and mass spectrometry was used in the present study to analyze the differentially expressed proteins. Samples from 21 patients (9 females and 12 males; mean age: 61.8 years) were used. We identified 18 differentially expressed proteins in CAG compared with matched normal mucosa. Eight proteins were up-regulated and 10 down-regulated in CAG when compared with the same amounts of proteins in individually matched normal gastric mucosa. Two novel proteins, proteasome activator subunit 1 (PSME1), which was down-regulated in CAG, and ribosomal protein S12 (RPS12), which was up-regulated in CAG, were further investigated. Their expression was validated by Western blot and RT-PCR in 15 CAG samples matched with normal mucosa. The expression level of RPS12 was significantly higher in CAG than in matched normal gastric mucosa (P < 0.05). In contrast, the expression level of PSME1 in CAG was significantly lower than in matched normal gastric mucosa (P < 0.05). This study clearly demonstrated that there are some changes in protein expression between CAG and normal mucosa. In these changes, down-regulation of PSME1 and up-regulation of RPS12 could be involved in the development of CAG. Thus, the differentially expressed proteins might play important roles in CAG as functional molecules.
| S-EPMC3854201 | biostudies-literature
Project description:Background/aimTo use liquid chromatography-mass spectrometry (LC-MS) to identify endogenous differential metabolites in the urine of rats with chronic atrophic gastritis (CAG).Materials and methodsMethylnitronitrosoguanidine (MNNG) was used to produce a CAG model in Wistar rats, and HE staining was used to determine the pathological model. LC-MS was used to detect the differential metabolic profiles in rat urine. Diversified analysis was performed by the statistical method.ResultsCompared with the control group, the model group had 68 differential metabolites, 25 that were upregulated and 43 that were downregulated. The main metabolic pathways were D-glutamine and D-glutamic acid metabolism, histidine metabolism and purine metabolism.ConclusionBy searching for differential metabolites and metabolic pathways in the urine of CAG rats, this study provides effective experimental data for the pathogenesis and clinical diagnosis of CAG.
| S-EPMC7657567 | biostudies-literature
Project description:The aim of this study was to identify prognosis-related differentially expressed lncRNAs and mRNAs in chronic atrophic gastritis (CAG). By analysis of high-throughput whole-transcriptome sequencing data, the levels of lncRNAs and mRNAs between CAG and chronic non-atrophic gastritis were compared pairwisely. In total, 97,282 lncRNA transcripts and 20,307 mRNA transcripts were acquired, including 50 upregulated and 66 downregulated lncRNAs and 377 upregulated and 763 downregulated mRNAs in CAG (p < 0.05, fold change ? 2). Moreover, the interactions of the differentially expressed genes in CAG were investigated by gene ontology enrichment analysis, showing that the enriched genes are involved in many biological processes, such as MAP kinase activity, heat generation, and protein modification processes. Through the construction of co-expression networks of the differentially expressed genes in CAG, three critical lncRNAs nodes were identified as potential key factors in CAG. Eight mRNAs common in both the co-expression network and the protein-protein interaction network were selected via Venn analysis, including DGKA, EIF6, HKDC1, DHRS11, 1, KRT15, TESPA1, and CDHR2. Finally, the expression levels of five differentially expressed lncRNAs in CAG were confirmed by quantitative real-time polymerase chain reaction. In conclusion, this study presents novel promising biomarkers for the diagnosis of CAG.
| S-EPMC7831747 | biostudies-literature
Project description:Chronic gastritis (CG) and osteoporosis (OP) are common and occult diseases in the elderly and the relationship of these two diseases have been increasingly exposed. We aimed to explore the clinical characteristics and shared mechanisms of CG patients combined with OP. In the cross-sectional study, all participants were selected from BEYOND study. The CG patients were included and classified into two groups, namely OP group and non-OP group. Univariable and multivariable logistic regression methods were used to evaluate the influencing factors. Furthermore, CG and OP-related genes were obtained from Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were identified using the GEO2R tool and the Venny platform. Protein-protein interaction information was obtained by inputting the intersection targets into the STRING database. The PPI network was constructed by Cytoscape v3.6.0 software again, and the key genes were screened out according to the degree value. Gene function enrichment of DEGs was performed by Webgestalt online tool. One hundred and thirty CG patients were finally included in this study. Univariate correlation analysis showed that age, gender, BMI and coffee were the potential influencing factors for the comorbidity (P < 0.05). Multivariate Logistic regression model found that smoking history, serum PTH and serum β-CTX were positively correlated with OP in CG patients, while serum P1NP and eating fruit had an negative relationship with OP in CG patients. In studies of the shared mechanisms, a total of 76 intersection genes were identified between CG and OP, including CD163, CD14, CCR1, CYBB, CXCL10, SIGLEC1, LILRB2, IGSF6, MS4A6A and CCL8 as the core genes. The biological processes closely related to the occurrence and development of CG and OP mainly involved Ferroptosis, Toll-like receptor signaling pathway, Legionellosis and Chemokine signaling pathway. Our study firstly identified the possible associated factors with OP in the patients with CG, and mined the core genes and related pathways that could be used as biomarkers or potential therapeutic targets to reveal the shared mechanisms.
| S-EPMC10042850 | biostudies-literature
Project description:The aims of this study are to identify prognosis-related differentially expressed lncRNAs and mRNAs in chronic atrophic gastritis (CAG). By analysis of high-throughput whole-transcriptome sequencing data, levels of lncRNAs and mRNAs between CAG and chronic nonatrophic gastritis (CNAG) were compared pairwisely. Finally, 97,282 lncRNA transcripts and 20,307 mRNA transcripts were acquired, including 50 upregulated and 66 downregulated lncRNAs and 377 upregulated and 763 downregulated mRNAs in CAG were identified (P< 0.05, fold change ≥2). Moreover, the interactions of the differentially expressed genes in CAG were investigated by gene ontology (GO) enrichment analysis, showing that the enriched genes are involved in many biological processes, such as MAP kinase activity, heat generation, and protein modification processes. Through the construction of co-expression networks of the differentially expressed genes in CAG, three critical lncRNAs nodes were identified as potential key factors in CAG. Eight mRNAs common in both the co-expression network and the protein-protein interaction (PPI) network were selected via Venn analysis, including DGKA, EIF6, HKDC1, DHRS11, CPS1, KRT15, TESPA1, and CDHR2.Finally, the expression levels of five differentially expressed lncRNAs in CAG were confirmed by quantitative real-time polymerase chain reaction (qRT-PCR). In conclusion, this study presents novel promising biomarkers for the diagnosis of CAG.
2021-02-02 | GSE153224 | GEO
Project description:Campylobacter fetus is a cause of enteritis and invasive extraintestinal disease in humans. In order to develop an animal model of C. fetus infection, outbred ICR SCID mice were orally challenged with a clinical isolate of C. fetus. The stomachs of SCID mice were heavily colonized with C. fetus, and colonization was associated with the development of chronic atrophic gastritis. This lesion was characterized by an inflammatory infiltrate of granulocytes and macrophages that over time resulted in a loss of specialized parietal and chief cells in the corpus and the appearance of a metaplastic mucous epithelium. This lesion bears similarity to that encountered during experimental murine infection with Helicobacter pylori or Helicobacter felis. Despite colonization of the cecum and colon tissues by C. fetus in SCID mice, no lesions were noted in these tissues. A follow-up study confirmed these findings for SCID mice and also demonstrated that C. fetus could also infect the gastric mucosa of wild-type, outbred ICR mice. However, in ICR mice, the anatomic extent of colonization was more limited and the severity of inflammation and epithelial alterations was significantly less than that observed in infected SCID mice. The stomach may represent an unrecognized environmental niche for Campylobacter species.
| S-EPMC97392 | biostudies-literature
Project description:Chronic gastritis is an inflammation of the gastric mucosa and has multiple etiologies. Here we discuss the pathological alterations induced by Helicobacter pylori (HP) leading to chronic gastritis and the epigenetic bases underlying these changes. We review the histology of the normal gastric mucosa and overview the role of HP in the multistep cascade of GC. We attempt to define the role of the Operative Link for Gastritis Assessment (OLGA) staging system in assessing the risk of GC. The epigenetic bases of chronic gastritis, mainly DNA methylation, are presented through examples such as (i) the methylation of the promoter region of E-cadherin in HP-induced chronic gastritis and its reversion after HP eradication and (ii) the association of methylation of the promoter region of Reprimo, a p53-mediated cell cycle arrest gene, with aggressive HP strains in high risk areas for GC. In addition, we discuss the finding of RPRM as a circulating cell-free DNA, offering the opportunity for noninvasive risk assessment of GC. Finally, the integration of OLGA and tissue biomarkers, by systems pathology approach, suggests that severe atrophy has a greater risk for GC development if, in addition, overexpressed p73. This trial is registered with ClinicalTrials.gov NCT01774266.
| S-EPMC3745848 | biostudies-literature
Project description:Helicobacter pylori infection can induce gastric pathologies ranging from chronic gastritis to peptic ulcers and gastric cancer. Individuals´ response to H. pylori infection is complex and it depends on a combination of environmental factors, genetic background, host response and strain virulence. The pathway towards gastric cancer is a sequence of events known as the Correa's model of gastric carcinogenesis, a stepwise inflammatory process from normal mucosa to chronic active gastritis, atrophy, metaplasia and finally gastric adenocarcinoma. This study explores gastric clinical specimens representing different steps of the Correa pathway with the aim of identifying the expression profile of coding- and non-coding RNAs (microRNAs and small RNAs) which may have a role in the Correa's model of gastric carcinogenesis and potentially develop novel clinical biomarkers. We screened for differentially expressed genes in gastric biopsies (antrum/corpus) by employing RNAseq (for microRNAs and non-coding RNAs) and microarrays (for coding RNAs).
2020-09-01 | E-MTAB-8889 | biostudies-arrayexpress
Project description:Helicobacter pylori infection can induce gastric pathologies ranging from chronic gastritis to peptic ulcers and gastric cancer. Individuals´ response to H. pylori infection is complex and it depends on a combination of environmental factors, genetic background, host response and strain virulence. The pathway towards gastric cancer is a sequence of events known as the Correa's model of gastric carcinogenesis, a stepwise inflammatory process from normal mucosa to chronic active gastritis, atrophy, metaplasia and finally gastric adenocarcinoma. This study explores gastric clinical specimens representing different steps of the Correa pathway with the aim of identifying the expression profile of coding- and non-coding RNAs (microRNAs and small RNAs) which may have a role in the Correa's model of gastric carcinogenesis and potentially develop novel clinical biomarkers. We screened for differentially expressed genes in gastric biopsies (antrum/corpus) by employing RNAseq (for microRNAs and non-coding RNAs) and microarrays (for coding RNAs).
2020-09-01 | E-MTAB-8890 | biostudies-arrayexpress
Project description:Gastric cancer is an important health problem because it is difficult to diagnose and treat in advanced stage. This makes that the prognosis of gastric cancer patients remains scarce. Currently it is known that the cause of gastric cancer is attributed to chronic infection with Helicobacter pylori. Its persistent infection leads to development of chronic atrophic gastritis that is considered as a predecessor stage of intestinal-type gastric cancer. The understanding of the alteration of molecular mechanisms during the early stages of the development of gastric cancer, and the identification of their potential biomarkers can allow a rapid diagnosis that leads to an improvement diagnosis and increase the patient’s prognosis. We analyzed gene expression profiles of patients with chronic atrophic gastritis and gastric cancer through microarray analysis, functional enrichment analysis and validation of gene expression by quantitative PCR. Gene expression profiles in patients with chronic atrophic gastritis showed molecular changes of the gastric mucosa, which leads to intestinal metaplasia and subsequently, gastric cancer. In gastric cancer the gene expression profile showed the stage of tumor progression, the product of these genes are potential biomarkers of early stages of cancer that can be potential therapeutic targets. Accordingly, the transcriptome analysis revealed several gene groups are related to development of chronic atrophic gastritis, some of which were inhibited in gastric cancer patients. The increased expression of CLDN1, CLDN7, OLFM4, c-Myc and MMP-9 genes in chronic atrophic gastritis and gastric cancer point outs to their use as promising biomarkers for the early diagnosis of gastric cancer.
2019-12-18 | GSE116312 | GEO