ArticleInflammation2012
HMGB1 increases permeability of the endothelial cell monolayer via RAGE and Src family tyrosine kinase pathways.
Article in Inflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
44 citing papers in PubMed, 87 citations in OpenAlex.
- High HMGB1 levels in sputum are related to pneumococcal bacteraemia but not to disease severity in community-acquired pneumonia.Scientific reports · 2018Trial
- Coronary Microvascular Dysfunction Is Associated With Augmented Lysosomal Signaling in Hypercholesterolemic Mice.Journal of the American Heart Association · 2024Article
- Endothelial Dysfunction with Aging: Does Sex Matter?International journal of molecular sciences · 2024Article
- Coronary Microvascular Dysfunction is Associated with Augmented Lysosomal Signaling in Hypercholesterolemic Mice.bioRxiv : the preprint server for biology · 2024Article
- Urolithin A-mediated augmentation of intestinal barrier function through elevated secretory mucin synthesis.Scientific reports · 2024Article
- Heparan sulfates and heparan sulfate binding proteins in sepsis.Frontiers in molecular biosciences · 2023Review
- MicroRNA 573 Rescues Endothelial Dysfunction during Dengue Virus Infection under PPARγ Regulation.Journal of virology · 2022Article
- The Role of NLRP3 Inflammasome in Diabetic Cardiomyopathy and Its Therapeutic Implications.Oxidative medicine and cellular longevity · 2022Review
- Hepatic small extracellular vesicles promote microvascular endothelial hyperpermeability during NAFLD via novel-miRNA-7.Journal of nanobiotechnology · 2021Article
- Targeting Cytokines, Pathogen-Associated Molecular Patterns, and Damage-Associated Molecular Patterns in Sepsis via Blood Purification.International journal of molecular sciences · 2021Review
- Regulation of vascular permeability in cancer metastasis.Cancer science · 2021Review
- High molecular weight sodium hyaluronate improves survival of syndecan-1-deficient septic mice by inhibiting neutrophil migration.PloS one · 2021Article
- Endothelial activation and dysfunction in COVID-19: from basic mechanisms to potential therapeutic approaches.Signal transduction and targeted therapy · 2020Review
- Sirtuin 1-dependent regulation of high mobility box 1 in hypoxia-reoxygenated brain microvascular endothelial cells: roles in neuronal amyloidogenesis.Cell death & disease · 2020Article
- The role of RAGE in host pathology and crosstalk between RAGE and TLR4 in innate immune signal transduction pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Review
- Nuclear Alarmin Cytokines in Inflammation.Journal of immunology research · 2020Review
- Article
- Contribution of cathepsin B-dependent Nlrp3 inflammasome activation to nicotine-induced endothelial barrier dysfunction.European journal of pharmacology · 2019Article
- Soluble RAGE attenuates AngII-induced endothelial hyperpermeability by disrupting HMGB1-mediated crosstalk between AT1R and RAGE.Experimental & molecular medicine · 2019Article
- High Mobility Group Box 1 Mediates TMAO-Induced Endothelial Dysfunction.International journal of molecular sciences · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High-mobility group box 1 (HMGB1) was recently established as a proinflammatory mediator of sepsis, and its potential role in the pathogenesis of sepsis remains elusive. In the present study, we determined whether HMGB1 increases the permeability of the endothelial cell monolayer in sepsis. Permeability was measured from fluorescein isothiocyanate (FITC)-dextran 40-kDa flux across the endothelial cell monolayer at control and after HMGB1 administration. We found that HMGB1 increased human umbilical vein endothelial cell permeability to FITC-dextran 40 kDa in a time- and concentration-dependent manner. HMGB1 induced the mRNA transcription and protein expression of receptor for advanced glycation end products (RAGE). Blockade of cell surface receptors RAGE with specific neutralizing antibodies and RAGE siRNA or blockade of Src family tyrosine kinase with inhibitor PP2 significantly reduced HMGB1-induced hyperpermeability of endothelial cell monolayer. Our data demonstrate that (1) HMGB1 increases permeability of endothelial cell monolayer in a time- and concentration-dependent manner and (2) HMGB1-induced hyperpermeability is mediated through RAGE and Src family tyrosine kinase signaling pathway. These findings may have implications for therapeutic interventions in patients with sepsis.
Indexed as
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.