ArticleCell death discovery2015
Helicobacter pylori VacA induces apoptosis by accumulation of connexin 43 in autophagic vesicles via a Rac1/ERK-dependent pathway.
Article in Cell death discovery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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Who cites it
35 citing papers in PubMed, 58 citations in OpenAlex.
- The miR-744-5p/connexin 43 axis modulates Salmonella-containing vacuole association with the Golgi network.The EMBO journal · 2026Article
- Review
- Mitochondrial Stress inAntioxidants (Basel, Switzerland) · 2026Review
- Rac1 in gastric cancer: a molecular driver of invasion, EMT, and therapeutic resistance.Journal of translational medicine · 2025Review
- Article
- Taurine modulates host cell responses toInfection and immunity · 2024Article
- Identification of potential drug candidates to treat gastritis and associated oxidative stress based on some novel 2-aryl-1RSC advances · 2024Article
- There Are No Insurmountable Barriers: Passage of theMembranes · 2023Review
- The interaction between autophagy, Helicobacter pylori, and gut microbiota in gastric carcinogenesis.Trends in microbiology · 2023Review
- Reactive Oxygen Species andAntioxidants (Basel, Switzerland) · 2023Review
- Restoration of mitochondrial structure and function withinAdvances in microbiology · 2023Article
- Review
- Microbe-host interactions: structure and functions of Gram-negative bacterial membrane vesicles.Frontiers in microbiology · 2023Review
- Establishment and Methodological Evaluation of a Method for Rapid Detection ofInfection and drug resistance · 2023Article
- The Microbiome in Gastrointestinal Cancers.Gastroenterology clinics of North America · 2022Review
- The crosstalk between bacteria and host autophagy: host defense or bacteria offense.Journal of microbiology (Seoul, Korea) · 2022Review
- Bacteria-Mediated Oncogenesis and the Underlying Molecular Intricacies: What We Know So Far.Frontiers in oncology · 2022Review
- Autophagy induced by H. pylori VacA regulated the survival mechanism of the SGC7901 human gastric cancer cell line.Genes & genomics · 2021Article
- Interplay and cooperation of Helicobacter pylori and gut microbiota in gastric carcinogenesis.BMC microbiology · 2021Review
- Autophagy in Gastric Mucosa: The Dual Role and Potential Therapeutic Target.BioMed research international · 2021Review
Corrections and comments
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Authors and funding
10 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori (H. pylori) produces vacuolating cytotoxin (VacA), a potent protein toxin, which is associated with gastric inflammation and ulceration. Recent studies demonstrated that connexins (Cxs), which are responsible for intracellular communication at gap junctions (GJs) as well as cell homeostasis, participate in VacA-induced cell death. We now demonstrate in AZ-521 cells that VacA increased cytoplasmic Cx43, accompanied by LC3-II generation in a time- and dose-dependent manner without induction of Cx43 mRNA expression. Inhibition of VacA-induced Rac1 activity prevented ERK phosphorylation and the increase in Cx43. Suppression of ERK activity and addition of N-acetyl-cysteine inhibited VacA-dependent increase in Cx43 and LC3-II. DIDS, an anion-selective inhibitor, suppressed VacA-dependent increase in Cx43, suggesting that VacA channel activity was involved in this pathway. By confocal microscopy, Cx43 increased by VacA was predominately localized in cholesterol-rich, detergent-resistant membranes including GJs, and a fraction of Cx43 was incorporated in endocytotic vesicles and autophagolysosomes. Accumulation of Cx43 was also observed in gastric mucosa from H. pylori-infected patients compared with healthy controls, suggesting that the pathogen caused a similar effect in vivo. Our findings show that VacA-mediated effects on autophagy inhibits turnover of Cx43, resulting in increased levels in the cytoplasm, leading eventually to apoptotic cell death.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.