ArticleJournal of inflammation (London, England)2008
Anti-oxidant inhibition of hyaluronan fragment-induced inflammatory gene expression.
Article in Journal of inflammation (London, England), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
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Who cites it
23 citing papers in PubMed, 53 citations in OpenAlex.
- Activated cardiac fibroblasts are a primary source of high-molecular-weight hyaluronan production.American journal of physiology. Cell physiology · 2025Article
- Targeting of Glycosaminoglycans in Genetic and Inflammatory Airway Disease.International journal of molecular sciences · 2022Review
- Cross-linked hyaluronic acid slows down collagen membrane resorption in diabetic rats through reducing the number of macrophages.Clinical oral investigations · 2022Article
- Damage-Associated Molecular Patterns in Myocardial Infarction and Heart Transplantation: The Road to Translational Success.Frontiers in immunology · 2020Review
- The Non-Fibrillar Side of Fibrosis: Contribution of the Basement Membrane, Proteoglycans, and Glycoproteins to Myocardial Fibrosis.Journal of cardiovascular development and disease · 2019Review
- Fragmented hyaluronan has no alarmin function assessed in arthritis synovial fibroblast and chondrocyte cultures.Innate immunity · 2018Article
- In vitro effects of hyaluronic acid on human periodontal ligament cells.BMC oral health · 2017Article
- Recent advances in orally administered cell-specific nanotherapeutics for inflammatory bowel disease.World journal of gastroenterology · 2016Review
- Activation of ERK and NF-κB during HARE-Mediated Heparin Uptake Require Only One of the Four Endocytic Motifs.PloS one · 2016Article
- The where, when, how, and why of hyaluronan binding by immune cells.Frontiers in immunology · 2015Review
- Hyaluronan, Inflammation, and Breast Cancer Progression.Frontiers in immunology · 2015Review
- Hyaluronan and cardiac regeneration.Journal of biomedical science · 2014Review
- Fluoride increases superoxide production and impairs the respiratory chain in ROS 17/2.8 osteoblastic cells.PloS one · 2014Article
- Activation of the FGFR-STAT3 pathway in breast cancer cells induces a hyaluronan-rich microenvironment that licenses tumor formation.Cancer research · 2014Article
- The hyaluronan receptor for endocytosis (HARE) activates NF-κB-mediated gene expression in response to 40-400-kDa, but not smaller or larger, hyaluronans.The Journal of biological chemistry · 2013Article
- Hyaluronidase facilitated subcutaneous immunoglobulin in primary immunodeficiency.ImmunoTargets and therapy · 2013Review
- Low-dosage metronomic chemotherapy and angiogenesis: topoisomerase inhibitors irinotecan and mitoxantrone stimulate VEGF-A-mediated angiogenesis.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2012Article
- Contact sensitizers induce skin inflammation via ROS production and hyaluronic acid degradation.PloS one · 2012Article
- Increased hyaluronan fragmentation during pulmonary ischemia.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- A novel unstable duplication upstream of HAS2 predisposes to a breed-defining skin phenotype and a periodic fever syndrome in Chinese Shar-Pei dogs.PLoS genetics · 2011Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThe balance between reactive oxygen species (ROS) and endogenous anti-oxidants is important in maintaining healthy tissues. Excessive ROS states occur in diseases such as ARDS and Idiopathic Pulmonary Fibrosis. Redox imbalance breaks down the extracellular matrix component hyaluronan (HA) into fragments that activate innate immune responses and perpetuate tissue injury. HA fragments, via a TLR and NF-kappaB pathway, induce inflammatory gene expression in macrophages and epithelial cells. NAC and DMSO are potent anti-oxidants which may help balance excess ROS states.
methodsWe evaluated the effect of H2O2, NAC and DMSO on HA fragment induced inflammatory gene expression in alveolar macrophages and epithelial cells.
resultsNAC and DMSO inhibit HA fragment-induced expression of TNF-alpha and KC protein in alveolar and peritoneal macrophages. NAC and DMSO also show a dose dependent inhibition of IP-10 protein expression, but not IL-8 protein, in alveolar epithelial cells. In addition, H2O2 synergizes with HA fragments to induce inflammatory genes, which are inhibited by NAC. Mechanistically, NAC and DMSO inhibit HA induced gene expression by inhibiting NF-kappaB activation, but NAC had no influence on HA-fragment-AP-1 mediated gene expression.
conclusionROS play a central role in a pathophysiologic "vicious cycle" of inflammation: tissue injury generates ROS, which fragment the extracellular matrix HA, which in turn synergize with ROS to activate the innate immune system and further promote ROS, HA fragment generation, inflammation, tissue injury and ultimately fibrosis. The anti-oxidants NAC and DMSO, by inhibiting the HA induced inflammatory gene expression, may help re-balance excessive ROS induced inflammation.
Identifiers
What OpenQuestion holds
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.