Pattern of Transcription Factor Activation in Helicobacter pylori–Infected Mongolian Gerbils

Kudo, Takahiko; Lü, Hong; Wu, Jeng‐Yih; Ohno, Tomoyuki; Wu, Michael; Genta, Robert M.; Graham, David Y.; Yamaoka, Yoshio

doi:10.1053/j.gastro.2007.01.009

Cited by 36 publications

(37 citation statements)

References 39 publications

(53 reference statements)

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“…The attenuation of this FRET with the inhibition of ERK activity that we detected indicates that the close approximation of the pc-Fos⅐c-Jun dimer depends on phosphorylation of ERK. Several studies have assessed potential AP-1 constituents in the response to H. pylori (27)(28)(29)(30)(31)(32), but in contrast to our study, they have not demonstrated the composition of the complex, the physical interaction of the components, the involvement of pc-Fos, or the role of AP-1 in apoptosis.…”

Section: Discussioncontrasting

confidence: 80%

“…In contrast, we found that inhibition of p38 had no effect and that interference with c-Fos phosphorylation with a dominant-negative plasmid completely attenuated the induction of apoptosis. Similarly, in studies in gastric epithelial cells (27)(28)(29)(30), the role of pc-Fos in AP-1 complex formation has not been assessed, and p38 as well as JNK have been implicated in the cytokine response, in contrast to our results in macrophages. Further, the role of pERK or AP-1 has not been previously studied in the setting of H. pylori-induced expression of c-Myc, ODC, or apoptosis in either macrophages or epithelial cells.…”

Section: Discussioncontrasting

confidence: 80%

“…Also nuclear extracts from H. pyloriinfected gerbil stomach tissues bind to the AP-1 consensus binding sequence (28). However, in both of these studies the constituents of the AP-1 complex were not determined.…”

mentioning

confidence: 95%

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Helicobacter pylori Induces ERK-dependent Formation of a Phospho-c-Fos·c-Jun Activator Protein-1 Complex That Causes Apoptosis in Macrophages

Asim

Chaturvedi

Hoge

et al. 2010

Journal of Biological Chemistry

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Macrophages are essential components of innate immunity, and apoptosis of these cells impairs mucosal defense to microbes. Helicobacter pylori is a gastric pathogen that infects half of the world population and causes peptic ulcer disease and gastric cancer. The host inflammatory response fails to eradicate the organism. We have reported that H. pylori induces apoptosis of macrophages by generation of polyamines from ornithine decarboxylase (

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Section: Discussioncontrasting

confidence: 80%

Section: Discussioncontrasting

confidence: 80%

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Helicobacter pylori Induces ERK-dependent Formation of a Phospho-c-Fos·c-Jun Activator Protein-1 Complex That Causes Apoptosis in Macrophages

Asim

Chaturvedi

Hoge

et al. 2010

Journal of Biological Chemistry

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“…The oipA gene encodes an extracellular inflammatory protein that is considered as a virulence factor for H pylori (Kudo et al, 2007). It is found that oipA gene is present in samples from stomach of significant percentage of patients with gastritis and gastric ulcers (Salih et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Investigation of Association between oipA and iceA1/iceA2 Genotypes of Helicobacter pylori and Gastric Cancer in Iran

Aghdam¹,

Sardari²,

Safaralizadeh³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Background: H pylori is the main causative agent of Gastric cancer and chronic gastritis. Genetic diversity of H. pylori has major contribution in its pathogenesis. We investigated the prevalence of oipA and iceA1/iceA2 positive strains of H. pylori among patients with gastric cancer and gastritis. Materials and Methods: Sampling performed by means of endoscopy from 86 patients. DNA was extracted from tissue samples using DNA extraction kit. PCR assay was performed and products were monitored by Agarose Gel Electrophoresis. Results: Urease Test and 16S rRNA PCR did not show significant differences in detection of H. pylori. The frequency of iceA1 allele in patients with gastric cancer was significantly higher than those with gastritis (p<0.05). However, there was no significant difference in prevalence of oipA and iceA2 genes among the two groups of patients (p>0.05). Conclusions: The iceA1 gene, but the oipA and iceA2 genes , is associated with H. pylori-induced gastric cancer. However, confirmatory studies must be performed in future.

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“…IL1B is a powerful pro-inflammatory cytokine that activates different transcription factors [19], some of which are also activated by H. pylori infection [20,21]. One of the IL1B-activated transcription factors is CCAAT/enhancer-binding protein beta (C/EBPb) [22].…”

Section: Introductionmentioning

confidence: 99%

Interleukin-1B signalling leads to increased survival of gastric carcinoma cells through a CREB-C/EBPβ-associated mechanism

et al. 2015

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Background Polymorphisms in inflammation-related genes have been associated with a risk of gastric carcinoma (GC). However, the biological mechanisms underlying these associations are still elusive. Our objective was to determine whether chronic inflammation-associated IL1B signalling, as seen in the context of Helicobacter pylori infection, could be linked to gastric carcinogenesis by modulating the behaviour of gastric epithelial cells. Methods The effect of IL1B was assessed by studying the expression and activation status of the IL1B-activated transcription factors C/EBPb and CREB in GC cell lines. Interaction between CREB and C/EBPb was explored through interference RNA, chromatin immunoprecipitation and chemical inhibition. CREB and C/EBPb expression was analysed in 66 samples of primary GC and in normal gastric mucosa. GC cell growth was analysed in vitro by BrdU incorporation and in vivo employing a chicken embryo chorioallantoic membrane model. Results We found that IL1B regulates the expression/ activation status of both C/EBPb and CREB in GC cells through an ERK1/2-dependent mechanism. Our results show that CREB is a direct transactivator of CEBPB, acting as an upstream effector in this regulatory mechanism. Furthermore, we found CREB to be overexpressed in 94 % of GC samples and significantly associated with C/EBPb expression (P \ 0.05). Finally, we demonstrated both in vitro and in vivo that CREB can mediate IL1B-induced GC cell proliferation. Conclusions Our results support the hypothesis that the effect of chronic inflammation on gastric carcinogenesis, as seen in the context of genetically susceptible individuals infected with Helicobacter pylori, includes the modulation of signalling pathways that regulate survival mechanisms in epithelial cells. Summary IL1B is able to increase the expression/activation status of CREB and its target gene C/EBPb, which are mandatory for GC cell survival. Our results may help inform new strategies for the prevention and treatment of GC, including the control of chronic inflammation.

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Pattern of Transcription Factor Activation in Helicobacter pylori–Infected Mongolian Gerbils

Cited by 36 publications

References 39 publications

Helicobacter pylori Induces ERK-dependent Formation of a Phospho-c-Fos·c-Jun Activator Protein-1 Complex That Causes Apoptosis in Macrophages

Helicobacter pylori Induces ERK-dependent Formation of a Phospho-c-Fos·c-Jun Activator Protein-1 Complex That Causes Apoptosis in Macrophages

Investigation of Association between oipA and iceA1/iceA2 Genotypes of Helicobacter pylori and Gastric Cancer in Iran

Interleukin-1B signalling leads to increased survival of gastric carcinoma cells through a CREB-C/EBPβ-associated mechanism

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