ArticleExperimental & molecular medicine2019
Soluble RAGE attenuates AngII-induced endothelial hyperpermeability by disrupting HMGB1-mediated crosstalk between AT1R and RAGE.
Article in Experimental & molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 57 citations in OpenAlex.
- Hydrogen sulfide improves vascular endothelial function in hypertensive states through SIRT6 anti-inflammatory signaling.Acta biochimica et biophysica Sinica · 2025Article
- Oxidative Stress and Endothelial Dysfunction: The Pathogenesis of Pediatric Hypertension.International journal of molecular sciences · 2025Review
- The Role of Alarmins in the Pathogenesis of Atherosclerosis and Myocardial Infarction.Current issues in molecular biology · 2024Review
- esRAGE-expressing oHSV enhances anti-tumor efficacy by inhibition of endothelial cell activation.Molecular therapy oncolytics · 2023Article
- Activation of immune signals during organ transplantation.Signal transduction and targeted therapy · 2023Review
- RAGE signaling regulates the progression of diabetic complications.Frontiers in pharmacology · 2023Review
- The short-chain fatty acid butyrate exerts a specific effect on VE-cadherin phosphorylation and alters the integrity of aortic endothelial cells.Frontiers in cell and developmental biology · 2023Article
- Evidence for Interplay Between the Renin-Angiotensin System and Toll-Like Receptor 4 Signaling Pathways in the Induction of Virus-Induced Acute Lung Injury.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022Article
- Methylglyoxal and Its Adducts: Induction, Repair, and Association with Disease.Chemical research in toxicology · 2022Review
- Review
- An imbalance between RAGE/MR/HMGB1 and ATP1α3 is associated with inflammatory changes in rat brain harboring cerebral aneurysms prone to rupture.Journal of neuroinflammation · 2022Article
- Circulating levels of AGEs and soluble RAGE isoforms are associated with all-cause mortality and development of cardiovascular complications in type 2 diabetes: a retrospective cohort study.Cardiovascular diabetology · 2022Article
- Downregulation of the endothelial histone demethylase JMJD3 is associated with neointimal hyperplasia of arteriovenous fistulas in kidney failure.The Journal of biological chemistry · 2022Article
- Measuring of Advanced Glycation End Products in Acute Stroke Care: Skin Autofluorescence as a Predictor of Ischemic Stroke Outcome in Patients with Diabetes Mellitus.Journal of clinical medicine · 2022Article
- In Vitro Methodologies to Study the Role of Advanced Glycation End Products (AGEs) in Neurodegeneration.Nutrients · 2022Review
- Loss of Id3 (Inhibitor of Differentiation 3) Increases the Number of IgM-Producing B-1b Cells in Ischemic Skeletal Muscle Impairing Blood Flow Recovery During Hindlimb Ischemia.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- RAGE pathway activation and function in chronic kidney disease and COVID-19.Frontiers in medicine · 2022Review
- Research progress in endothelial cell injury and repair.Frontiers in pharmacology · 2022Review
- Hyperactivated RAGE in Comorbidities as a Risk Factor for Severe COVID-19-The Role of RAGE-RAS Crosstalk.Biomolecules · 2021Review
- Targeting RAGE to prevent SARS-CoV-2-mediated multiple organ failure: Hypotheses and perspectives.Life sciences · 2021Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Increased endothelial permeability, one of the earliest signs of endothelial dysfunction, is associated with the development of cardiovascular diseases such as hypertension and atherosclerosis. Recent studies suggest that the receptor for advanced glycation end products (RAGE) regulates endothelial permeability in inflammation. In the present study, we investigated the regulatory mechanism of RAGE in endothelial hyperpermeability induced by angiotensin II (Ang II), a well-known inflammatory mediator, and the potential therapeutic effect of soluble RAGE (sRAGE), a decoy receptor for RAGE ligands. For in vitro studies, Ang II-treated human umbilical vein endothelial cells (HUVECs) were treated with siRNA specific to either RAGE or sRAGE to disrupt RAGE-mediated signaling. Endothelial permeability was estimated using FITC-labeled dextran 40 and a resistance meter. To evaluate intercellular junction disruption, VE-cadherin expression was examined by western blotting and immunocytochemistry. Ang II increased the expression of the Ang II type 1 receptor (AT1R) and RAGE, and this increase was inhibited by sRAGE. sRAGE prevented Ang II-induced VE-cadherin disruption in HUVECs. For in vivo studies, Ang II-infused, atherosclerosis-prone apolipoprotein E knockout mice were utilized. Endothelial permeability was assessed by Evans blue staining of the aorta. Ang II increased endothelial barrier permeability, and this effect was significantly attenuated by sRAGE. Our data demonstrate that blockade of RAGE signaling using sRAGE attenuates Ang II-induced endothelial barrier permeability in vitro and in vivo and indicate the therapeutic potential of sRAGE in controlling vascular permeability under pathological conditions.
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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.