ArticlePLoS pathogens2013
Caveolin-1 protects B6129 mice against Helicobacter pylori gastritis.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Metabolic reprogramming as a key regulator in Helicobacter pylori-infected gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2026Review
- Caspase-11 contributes to site-1 protease cleavage and SREBP1 activation in the inflammatory response of macrophages.Frontiers in immunology · 2023Article
- Functional antagonism between CagA and DLC1 in gastric cancer.Cell death discovery · 2022Article
- The Role of Lipid Metabolism in Gastric Cancer.Frontiers in oncology · 2022Review
- Effect of β-caryophyllene from Cloves Extract onNutrients · 2020Article
- Caveolae as Potential Hijackable Gates in Cell Communication.Frontiers in cell and developmental biology · 2020Review
- Cell Intrinsic and Extrinsic Mechanisms of Caveolin-1-Enhanced Metastasis.Biomolecules · 2019Review
- Article
- All-trans retinoic acid inhibits the proliferation of SGC7901 cells by regulating caveolin-1 localization via the ERK/MAPK signaling pathway.Oncology letters · 2018Article
- DNA methylation as a marker of response in rheumatoid arthritis.Pharmacogenomics · 2017Review
- An epigenome-wide association study of inflammatory response to fenofibrate in the Genetics of Lipid Lowering Drugs and Diet Network.Pharmacogenomics · 2017Article
- Cooperation of Gastric Mononuclear Phagocytes withJournal of immunology (Baltimore, Md. : 1950) · 2017Article
- Article
- Role of Helicobacter pylori infection in pathogenesis of gastric carcinoma.World journal of gastrointestinal pathophysiology · 2016Review
- Downregulation of caveolin-1 in chronic rhinosinusitis with and without nasal polyps.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2015Article
- Caveolin-1 is a modulator of fibroblast activation and a potential biomarker for gastric cancer.International journal of biological sciences · 2015Article
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Authors and funding
12 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Caveolin-1 (Cav1) is a scaffold protein and pathogen receptor in the mucosa of the gastrointestinal tract. Chronic infection of gastric epithelial cells by Helicobacter pylori (H. pylori) is a major risk factor for human gastric cancer (GC) where Cav1 is frequently down-regulated. However, the function of Cav1 in H. pylori infection and pathogenesis of GC remained unknown. We show here that Cav1-deficient mice, infected for 11 months with the CagA-delivery deficient H. pylori strain SS1, developed more severe gastritis and tissue damage, including loss of parietal cells and foveolar hyperplasia, and displayed lower colonisation of the gastric mucosa than wild-type B6129 littermates. Cav1-null mice showed enhanced infiltration of macrophages and B-cells and secretion of chemokines (RANTES) but had reduced levels of CD25+ regulatory T-cells. Cav1-deficient human GC cells (AGS), infected with the CagA-delivery proficient H. pylori strain G27, were more sensitive to CagA-related cytoskeletal stress morphologies ("humming bird") compared to AGS cells stably transfected with Cav1 (AGS/Cav1). Infection of AGS/Cav1 cells triggered the recruitment of p120 RhoGTPase-activating protein/deleted in liver cancer-1 (p120RhoGAP/DLC1) to Cav1 and counteracted CagA-induced cytoskeletal rearrangements. In human GC cell lines (MKN45, N87) and mouse stomach tissue, H. pylori down-regulated endogenous expression of Cav1 independently of CagA. Mechanistically, H. pylori activated sterol-responsive element-binding protein-1 (SREBP1) to repress transcription of the human Cav1 gene from sterol-responsive elements (SREs) in the proximal Cav1 promoter. These data suggested a protective role of Cav1 against H. pylori-induced inflammation and tissue damage. We propose that H. pylori exploits down-regulation of Cav1 to subvert the host's immune response and to promote signalling of its virulence factors in host cells.
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