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Gene expression profiling in gastric mucosa from Helicobacter pylori-infected and uninfected patients undergoing chronic superficial gastritis.

Yang ZM, Chen WW, Wang YF - PLoS ONE (2012)

Bottom Line: The annotated genes were involved in protein metabolism, inflammatory and immunological reaction, signal transduction, gene transcription, trace element metabolism, and so on.The 82% of these genes (28/34) were categorized in three molecular interaction networks involved in gene expression, cancer progress, antigen presentation and inflammatory response.The expression data of the array hybridization was confirmed by quantitative real-time PCR assays.

View Article: PubMed Central - PubMed

Affiliation: Pi-Wei Institute, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.

ABSTRACT
Helicobacter pylori infection reprograms host gene expression and influences various cellular processes, which have been investigated by cDNA microarray using in vitro culture cells and in vivo gastric biopsies from patients of the Chronic Abdominal Complaint. To further explore the effects of H. pylori infection on host gene expression, we have collected the gastric antral mucosa samples from 6 untreated patients with gastroscopic and pathologic confirmation of chronic superficial gastritis. Among them three patients were infected by H. pylori and the other three patients were not. These samples were analyzed by a microarray chip which contains 14,112 cloned cDNAs, and microarray data were analyzed via BRB ArrayTools software and Ingenuity Pathways Analysis (IPA) website. The results showed 34 genes of 38 differentially expressed genes regulated by H. pylori infection had been annotated. The annotated genes were involved in protein metabolism, inflammatory and immunological reaction, signal transduction, gene transcription, trace element metabolism, and so on. The 82% of these genes (28/34) were categorized in three molecular interaction networks involved in gene expression, cancer progress, antigen presentation and inflammatory response. The expression data of the array hybridization was confirmed by quantitative real-time PCR assays. Taken together, these data indicated that H. pylori infection could alter cellular gene expression processes, escape host defense mechanism, increase inflammatory and immune responses, activate NF-κB and Wnt/β-catenin signaling pathway, disturb metal ion homeostasis, and induce carcinogenesis. All of these might help to explain H. pylori pathogenic mechanism and the gastroduodenal pathogenesis induced by H. pylori infection.

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Cluster diagram of differentially expressed genes in H. pylori-infected and uninfected patients undergoing chronic superficial gastritis.Each column represented one sample and each row represented one gene. Red indicated higher expression and green indicated lower expression. Blank in the row indicated that the differentially expressed UniGene ID had not been annotated.
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pone-0033030-g002: Cluster diagram of differentially expressed genes in H. pylori-infected and uninfected patients undergoing chronic superficial gastritis.Each column represented one sample and each row represented one gene. Red indicated higher expression and green indicated lower expression. Blank in the row indicated that the differentially expressed UniGene ID had not been annotated.

Mentions: We performed cluster analysis for the samples from six patients of chronic superficial gastritis and 38 differentially expressed genes using BRB ArrayTools software. For samples, the patients were divided into two clusters of H. pylori infected and uninfected. For genes, down-regulated genes were clustered into two groups with C5ORF53, SCGN, RNF138, ELP4, RWDD4A, ASB15, C19ORF2 and RNASEH2B in one group, while ATP6AP2, NR1D2, MUC16, GOLPH3, MST4 and SLC39A6 in the other group; up-regulated genes were also clustered into two groups. PSMD5, GPX1, WASH1, HDAC7, HLA-DRB1, RPS27, CEACAM8 and MED6 were clustered into one group, while the rest formed the other group (Figure 2).


Gene expression profiling in gastric mucosa from Helicobacter pylori-infected and uninfected patients undergoing chronic superficial gastritis.

Yang ZM, Chen WW, Wang YF - PLoS ONE (2012)

Cluster diagram of differentially expressed genes in H. pylori-infected and uninfected patients undergoing chronic superficial gastritis.Each column represented one sample and each row represented one gene. Red indicated higher expression and green indicated lower expression. Blank in the row indicated that the differentially expressed UniGene ID had not been annotated.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3306372&req=5

pone-0033030-g002: Cluster diagram of differentially expressed genes in H. pylori-infected and uninfected patients undergoing chronic superficial gastritis.Each column represented one sample and each row represented one gene. Red indicated higher expression and green indicated lower expression. Blank in the row indicated that the differentially expressed UniGene ID had not been annotated.
Mentions: We performed cluster analysis for the samples from six patients of chronic superficial gastritis and 38 differentially expressed genes using BRB ArrayTools software. For samples, the patients were divided into two clusters of H. pylori infected and uninfected. For genes, down-regulated genes were clustered into two groups with C5ORF53, SCGN, RNF138, ELP4, RWDD4A, ASB15, C19ORF2 and RNASEH2B in one group, while ATP6AP2, NR1D2, MUC16, GOLPH3, MST4 and SLC39A6 in the other group; up-regulated genes were also clustered into two groups. PSMD5, GPX1, WASH1, HDAC7, HLA-DRB1, RPS27, CEACAM8 and MED6 were clustered into one group, while the rest formed the other group (Figure 2).

Bottom Line: The annotated genes were involved in protein metabolism, inflammatory and immunological reaction, signal transduction, gene transcription, trace element metabolism, and so on.The 82% of these genes (28/34) were categorized in three molecular interaction networks involved in gene expression, cancer progress, antigen presentation and inflammatory response.The expression data of the array hybridization was confirmed by quantitative real-time PCR assays.

View Article: PubMed Central - PubMed

Affiliation: Pi-Wei Institute, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.

ABSTRACT
Helicobacter pylori infection reprograms host gene expression and influences various cellular processes, which have been investigated by cDNA microarray using in vitro culture cells and in vivo gastric biopsies from patients of the Chronic Abdominal Complaint. To further explore the effects of H. pylori infection on host gene expression, we have collected the gastric antral mucosa samples from 6 untreated patients with gastroscopic and pathologic confirmation of chronic superficial gastritis. Among them three patients were infected by H. pylori and the other three patients were not. These samples were analyzed by a microarray chip which contains 14,112 cloned cDNAs, and microarray data were analyzed via BRB ArrayTools software and Ingenuity Pathways Analysis (IPA) website. The results showed 34 genes of 38 differentially expressed genes regulated by H. pylori infection had been annotated. The annotated genes were involved in protein metabolism, inflammatory and immunological reaction, signal transduction, gene transcription, trace element metabolism, and so on. The 82% of these genes (28/34) were categorized in three molecular interaction networks involved in gene expression, cancer progress, antigen presentation and inflammatory response. The expression data of the array hybridization was confirmed by quantitative real-time PCR assays. Taken together, these data indicated that H. pylori infection could alter cellular gene expression processes, escape host defense mechanism, increase inflammatory and immune responses, activate NF-κB and Wnt/β-catenin signaling pathway, disturb metal ion homeostasis, and induce carcinogenesis. All of these might help to explain H. pylori pathogenic mechanism and the gastroduodenal pathogenesis induced by H. pylori infection.

Show MeSH
Related in: MedlinePlus