ArticleCell cycle (Georgetown, Tex.)2011
Caveolin-2-deficient mice show increased sensitivity to endotoxemia.
Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Downregulation of Caveolin-2 Is a Novel Mechanism Involved in Activation of Inducible Nitric Oxide Synthase (iNOS) in Mouse Peritoneal Macrophages.Mediators of inflammation · 2026Article
- Caveolin and oxidative stress in cardiac pathology.Frontiers in physiology · 2025Review
- Increased Caveolin-2 Expression in Brain Endothelial Cells Promotes Age-Related Neuroinflammation.Molecules and cells · 2022Article
- Elevated postischemic tissue injury and leukocyte-endothelial adhesive interactions in mice with global deficiency in caveolin-2: role of PAI-1.American journal of physiology. Heart and circulatory physiology · 2021Article
- Lung Endothelial Transcytosis.Comprehensive Physiology · 2020Review
- Toll-like Receptor 4 Signaling and Downstream Neutrophilic Inflammation Mediate Endotoxemia-Enhanced Blood-Labyrinth Barrier Trafficking.Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology · 2020Article
- Actin dynamics in the regulation of endothelial barrier functions and neutrophil recruitment during endotoxemia and sepsis.Cellular and molecular life sciences : CMLS · 2017Review
- Caveolae provide a specialized membrane environment for respiratory syncytial virus assembly.Journal of cell science · 2017Article
- Caveolin-1 and Caveolin-2 Can Be Antagonistic Partners in Inflammation and Beyond.Frontiers in immunology · 2017Review
- Size and dose dependent effects of silver nanoparticle exposure on intestinal permeability in an in vitro model of the human gut epithelium.Journal of nanobiotechnology · 2016Article
- Caveolae and Caveolin-1 Integrate Reverse Cholesterol Transport and Inflammation in Atherosclerosis.International journal of molecular sciences · 2016Review
- Host deficiency in caveolin-2 inhibits lung carcinoma tumor growth by impairing tumor angiogenesis.Cancer research · 2014Article
- Suppression of PTRF alleviates the polymicrobial sepsis induced by cecal ligation and puncture in mice.The Journal of infectious diseases · 2013Article
- Role of caveolin-1 and caveolae signaling in endotoxemia and sepsis.Life sciences · 2013Review
- Genetic ablation of caveolin-2 sensitizes mice to bleomycin-induced injury.Cell cycle (Georgetown, Tex.) · 2013Article
- Article
- Intestinal Salmonella typhimurium infection leads to miR-29a induced caveolin 2 regulation.PloS one · 2013Article
- Novel insights into the role of caveolin-2 in cell- and tissue-specific signaling and function.Biochemistry research international · 2011Article
- Role of Caveolin Proteins in Sepsis.Pediatrics & therapeutics : current researchArticle
- The Einstein-Brazil Fogarty: A decade of synergy.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology]Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Caveolin proteins are structural components of caveolae and are involved in the regulation of many biological processes. Recent studies have shown that caveolin-1 modulates inflammatory responses and is important for sepsis development. In the present study, we show that caveolin-1 and caveolin-2 have opposite roles in lipopolysaccharide (LPS)-induced sepsis using caveolin-deficient (Cav-1 (-/-) and Cav-2 (-/-) ) mice for each of these proteins. While Cav-1 (-/-) mice displayed delayed mortality following challenge with LPS, Cav-2 (-/-) mice were more sensitive to LPS compared to wild-type (WT). With Cav-2 (-/-) mice, this effect was associated with increased intestinal injury and increased intestinal permeability. This negative outcome was also correlated with enhanced expression of iNOS in epithelial intestinal cells, and enhanced production of nitric oxide (NO). By contrast, Cav-1 (-/-) mice demonstrated a decrease in iNOS expression with decreased NO production, but no alteration in intestinal permeability. The differential expression of iNOS was associated with a significant increase of STAT-1 activation in these mice. Intestinal cells of Cav-2 (-/-) mice showed increased phosphorylation of STAT-1 at tyrosine 701 compared to wild-type. However, Cav-1 (-/-) mice-derived intestinal cells showed decreased levels of phosphorylation of STAT-1 at tyrosine 701. Since caveolin-2 is almost completely absent in Cav-1 (-/-) mice, we conclude that it is not just the absence of caveolin-2 that is responsible for the observed effects, but that the balance between caveolin-1 and caveolin-2 is important for iNOS expression and ultimately for sepsis outcome.
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Registered trials
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