ArticleJournal of clinical biochemistry and nutrition2015
Repressed TGF-β signaling through CagA-Smad3 interaction as pathogenic mechanisms of Helicobacter pylori-associated gastritis.
Article in Journal of clinical biochemistry and nutrition, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- TGFβ1 induces CXCL1 to promote stemness features in lung cancer.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Review
- The correlation of Th22 and regulatory T cells with Helicobacter pylori infection in patients with chronic gastritis.Immunity, inflammation and disease · 2023Article
- Changes in Gastric Mucosal Glycosylation Before and After Helicobacter pylori Eradication Using Lectin Microarray Analysis.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2022Article
- Integrated analysis of Helicobacter pylori-related prognostic gene modification patterns in the tumour microenvironment of gastric cancer.Frontiers in surgery · 2022Article
- Transcriptome profiling analysis of the response to walnut polyphenol extract inJournal of clinical biochemistry and nutrition · 2021Article
- Berberine Attenuates Chronic Atrophic Gastritis Induced by MNNG and Its Potential Mechanism.Frontiers in pharmacology · 2021Article
- Arginase-1 and Treg Profile Appear to Modulate Inflammatory Process in Patients with Chronic Gastritis:Mediators of inflammation · 2019Article
- Microbial carcinogenic toxins and dietary anti-cancer protectants.Cellular and molecular life sciences : CMLS · 2017Review
- Quercetin from Polygonum capitatum Protects against Gastric Inflammation and Apoptosis Associated with Helicobacter pylori Infection by Affecting the Levels of p38MAPK, BCL-2 and BAX.Molecules (Basel, Switzerland) · 2017Article
- Characteristics of gastric cancer detected within 1 year after successful eradication ofJournal of clinical biochemistry and nutrition · 2016Article
- Esomeprazole- or rabeprazole-based triple therapy eradicatedJournal of clinical biochemistry and nutrition · 2016Article
- The expression of IGF-1R in Helicobacter pylori-infected intestinal metaplasia and gastric cancer.Journal of clinical biochemistry and nutrition · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori (H. pylori) infection causes chronic gastric inflammation, peptic ulceration, and gastric carcinogenesis, in which H. pylori cytotoxin-associated gene A (CagA) plays major pathogenic action. Since transforming growth factor-β (TGF-β) and its signaling also are principally implicated in either modulating gastric mucosal inflammatory responses or causing carcinogenesis and are attenuated after H. pylori infection, we hypothesized that dysregulated Smad signaling and repressed TGF-β might be core pathogenic mechanism for H. pylori-associated gastritis or carcinogenesis. Until now, no precise underlying mechanism how deranged TGF-β signaling developed after H. pylori infection relevant to various clinical manifestations remains unclear. In this study, we examined the molecular mechanism about the inhibition of TGF-β signaling by H. pylori CagA protein. H. pylori CagA significantly suppressed TGF-β/Smad transcriptional responses through critical inhibition of Smad3, though CagA interacted constitutively with Smad2, Smad3, and Smad4. CagA inhibited TGF-β-induced suppression of proinflammatory chemokines, such as IL-8, CXCL1 and CXCL3, as well as TGF-β-induced transcription of target genes. In conclusion, repressed TGF-β signaling associated with CagA-positive H. pylori infection could be an important determinant for the outcome of H. pylori infection. Therefore, TGF-β signaling is one of the important determinants to avoid from H. pylori CagA pathogenicity.
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