ArticleJournal of cellular physiology2018
HMGB1 contributes to the irradiation-induced endothelial barrier injury through receptor for advanced glycation endproducts (RAGE).
Article in Journal of cellular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- HMGB1 as a danger signal in vascular remodeling.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Review
- Discovery of Personalized Treatment for Immuno-Metabolic Depression-Focus on 11beta Hydroxysteroid Dehydrogenase Type 2 (11betaHSD2) and Toll-like Receptor 4 (TLR4) Inhibition with Enoxolone.Pharmaceuticals (Basel, Switzerland) · 2025Review
- CpG-A induces liquid-liquid phase separation of HMGB1 to activate the RAGE-mediated inflammatory pathway.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Novel Insights into the Mechanism and Treatment of Diabetes-Related Brain Complications: Focusing on the Blood-Brain Barrier Impairment.Aging and disease · 2025Review
- Protocatechuic Acid Ameliorates Cisplatin-Induced Inflammation and Apoptosis in Mouse Proximal Tubular Cells.International journal of molecular sciences · 2025Article
- Role of ferroptosis in the pathogenesis of heart disease.Frontiers in physiology · 2024Review
- Inhibition of HMGB1 Attenuates Spinal Cord Edema by Reducing the Expression of NaJournal of neurotrauma · 2023Article
- Cannabinoid receptor type 1 in the aging gut regulates the mucosal permeability via miR-191-5p.Frontiers in endocrinology · 2023Article
- Advances in the study of the molecular biological mechanisms of radiation-induced brain injury.American journal of cancer research · 2023Review
- In Vitro Methodologies to Study the Role of Advanced Glycation End Products (AGEs) in Neurodegeneration.Nutrients · 2022Review
- Anti-high-mobility group box-1 (HMGB1) mediates the apoptosis of alveolar epithelial cells (AEC) by receptor of advanced glycation end-products (RAGE)/c-Jun N-terminal kinase (JNK) pathway in the rats of crush injuries.Journal of orthopaedic surgery and research · 2022Article
- Cardiovascular Dysfunction in COVID-19: Association Between Endothelial Cell Injury and Lactate.Frontiers in immunology · 2022Review
- Glycyrrhizin ameliorating sterile inflammation induced by low-dose radiation exposure.Scientific reports · 2021Article
- The role of irreversible electroporation in promoting M1 macrophage polarization via regulating the HMGB1-RAGE-MAPK axis in pancreatic cancer.Oncoimmunology · 2021Article
- Receptor for Advanced Glycation End Products Is Involved in LPALife (Basel, Switzerland) · 2021Article
- Gamma Radiation Induce Inflammasome Signaling and Pyroptosis in Microvascular Endothelial Cells.Journal of inflammation research · 2021Article
- Roles of RAGE/ROCK1 Pathway in HMGB1-Induced Early Changes in Barrier Permeability of Human Pulmonary Microvascular Endothelial Cell.Frontiers in immunology · 2021Article
- Bile duct ligation enhances AZT CNS toxicity partly by impairing the expression and function of BCRP in rat brain.Acta pharmacologica Sinica · 2020Article
- HMGB1 in Radiotherapy: A Two Headed Signal Regulating Tumor Radiosensitivity and Immunity.OncoTargets and therapy · 2020Review
- Pathological effects of ionizing radiation: endothelial activation and dysfunction.Cellular and molecular life sciences : CMLS · 2019Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to investigate whether HMGB1 (high mobility group box-1 protein) and receptor for advanced glycation end products (RAGE) were involved in the irradiation-induced endothelial barrier damage and their mechanism. We constructed the damage model of endothelium barrier model with bEnd.3 cells. The permeability of endothelial barrier was detected by sodium fluorescein (Na-F) permeation test, and the irradiation dose which could induce permeability transition was determined by being exposed to different irradiation doses (5, 10, 15, 20 Gy). MTT assay was applied to detect cell viability under different concentrations of HMGB1, glycyrrhizic acid (GA, a specific inhibitor of HMGB1), and FPS-ZM1 (a blood-brain-barrier permeant blocker of RAGE V domain-mediated ligand binding). The expression of HMGB1, RAGE, and related molecules involved in MAPK signaling pathway, MMP-2, MMP-9, ZO-1, and claudin 5 of differently treated groups were measured by qRT-PCR, western blot, and immunofluorescence. Cells possessed stable endothelial barrier function on 4-7 days after seeded on transwell plates. The permeability of endothelial barrier would change under at least 10 Gy radiation. Both radiation and HMGB1 treatment alone could improve the permeability. After irradiation, the expressions of HMGB1 and RAGE increased and MAPK signal pathway was activated. Meanwhile, MMP-2 and MMP-9 were overexpressed, while the expression of tight junction proteins ZO-1 and claudin 5 was decreased. Radiation could activate MAPK signaling pathway through promoting the expression of HMGB1 and RAGE, which further led to endothelial barrier injury and changed its permeability.
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Registered trials
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