ArticleThe Journal of clinical investigation2007
Antiinflammatory adaptation to hypoxia through adenosine-mediated cullin-1 deneddylation.
Article in The Journal of clinical investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
57 citing papers in PubMed, 80 citations in OpenAlex.
- Immune consequences of exercise in hypoxia: A narrative review.Journal of sport and health science · 2024Review
- Regulatory mechanisms and therapeutic potential of JAB1 in neurological development and disorders.Molecular medicine (Cambridge, Mass.) · 2023Review
- The hypoxic tissue microenvironment as a driver of mucosal inflammatory resolution.Frontiers in immunology · 2023Review
- Hypoxia inducible factors regulate infectious SARS-CoV-2, epithelial damage and respiratory symptoms in a hamster COVID-19 model.PLoS pathogens · 2022Article
- Emerging role of protein modification in inflammatory bowel disease.Journal of Zhejiang University. Science. B · 2022Review
- The elegant complexity of mammalian ecto-5'-nucleotidase (CD73).Trends in cell biology · 2021Review
- Comparative Transcriptional Analysis of Pulmonary Arterial Hypertension Associated With Three Different Diseases.Frontiers in cell and developmental biology · 2021Article
- The pivotal roles of neddylation pathway in immunoregulation.Immunity, inflammation and disease · 2020Review
- Role of the COP9 Signalosome (CSN) in Cardiovascular Diseases.Biomolecules · 2019Review
- Control and dysregulation of redox signalling in the gastrointestinal tract.Nature reviews. Gastroenterology & hepatology · 2019Review
- Endogenous adenosine maintains cartilage homeostasis and exogenous adenosine inhibits osteoarthritis progression.Nature communications · 2017Article
- The Diverse Biological Functions of Neutrophils, Beyond the Defense Against Infections.Inflammation · 2017Review
- Actors and Factors in the Resolution of Intestinal Inflammation: Lipid Mediators As a New Approach to Therapy in Inflammatory Bowel Diseases.Frontiers in immunology · 2017Review
- Perturbation of neddylation-dependent NF-κB responses in the intestinal epithelium drives apoptosis and inhibits resolution of mucosal inflammation.Molecular biology of the cell · 2016Article
- Neutrophils and the inflammatory tissue microenvironment in the mucosa.Immunological reviews · 2016Review
- Hypoxia and Mucosal Inflammation.Annual review of pathology · 2016Review
- Targeting hypoxia in inflammatory bowel disease.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2016Review
- Molecular mechanisms of ischemic preconditioning in the kidney.American journal of physiology. Renal physiology · 2015Review
- Epithelial-specific A2B adenosine receptor signaling protects the colonic epithelial barrier during acute colitis.Mucosal immunology · 2015Article
- Neutrophils and inflammatory resolution in the mucosa.Seminars in immunology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
A major adaptive pathway for hypoxia is hypoxic preconditioning (HPC), a form of endogenous protection that renders cells tolerant to severe challenges of hypoxia. We sought to define the antiinflammatory properties of HPC. cDNA microarray analysis of lung tissue from mice subjected to hypoxia or HPC identified a cluster of NF-kappaB-regulated genes whose expression is attenuated by HPC. Studies using an NF-kappaB luciferase reporter assay confirmed a significant suppression of NF-kappaB activation during HPC. HPC-elicited activity was conferrable, as a soluble supernatant from HPC-treated cells, and the active fraction was purified and identified as adenosine (Ado). Guided by recent studies demonstrating bacterial inhibition of NF-kappaB through cullin-1 (Cul-1) deneddylation, we found a dose-dependent deneddylation of Cul-1 by Ado receptor stimulation predominantly mediated by the Ado A2B receptor subtype. Further, siRNA-mediated repression of CSN5, a subunit of the COP9 signalosome responsible for deneddylation of Cul-1, partially reversed HPC-mediated inhibition of NF-kappaB. Cul-1 deneddylation was evident in a murine model of HPC and lost in animals lacking extracellular Ado (Cd73-/- mice). Taken together, these results demonstrate that HPC induces extracellular accumulation of Ado and suppresses NF-kappaB activity through deneddylation of Cul-1. These results define a molecular regulatory pathway by which Ado provides potent antiinflammatory properties.
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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.