ArticleAmerican journal of physiology. Cell physiology2021
Changes in endothelial glycocalyx layer protective ability after inflammatory stimulus.
Article in American journal of physiology. Cell physiology, 2021. 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, 31 citations in OpenAlex.
- Evaluating the endothelial glycocalyx from bench to bedside: a translational framework for microvascular assessment.Angiogenesis · 2026Review
- Role of neutrophils in regulating vascular permeability in inflammatory and autoimmune diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Viral receptors as host-pathogen control nodes linking entry, signalling, and system-level pathogenesis.FEMS microbiology reviews · 2026Review
- Glycocalyx strengthens endothelial barrier function and protects from angioedema inducing compounds.Frontiers in immunology · 2026Article
- Endothelial barrier and sepsis: mechanisms and potential therapeutic strategies.Military Medical Research · 2026Review
- Association between glucosamine use and albuminuria in the UK: a cohort and Mendelian randomisation study.BMJ open · 2025Article
- Beyond the Hit: Muscle and Vascular Tissue Responses to Contact Exposure in Collision Sports-A Narrative Review.Sports medicine (Auckland, N.Z.) · 2025Review
- The glycocalyx: a key target for treatment of severe acute pancreatitis-associated multiple organ dysfunction syndrome.Human cell · 2025Review
- AMP dependent protein kinase regulates endothelial heparan sulfate expression in response to an inflammatory stimulus under arterial shear stress.Biochemical and biophysical research communications · 2024Article
- Sepsis-Induced Endothelial Dysfunction: Permeability and Regulated Cell Death.Journal of inflammation research · 2024Review
- The Pulmonary Endothelial Glycocalyx Modifications in Glypican 1 Knockout Mice Do Not Affect Lung Endothelial Function in Physiological Conditions.International journal of molecular sciences · 2023Article
- Crosstalk between Platelets and SARS-CoV-2: Implications in Thrombo-Inflammatory Complications in COVID-19.International journal of molecular sciences · 2023Review
- Matrix stiffness, endothelial dysfunction and atherosclerosis.Molecular biology reports · 2023Review
- The Shear Stress-Regulated Expression of Glypican-4 in Endothelial Dysfunction In Vitro and Its Clinical Significance in Atherosclerosis.International journal of molecular sciences · 2023Article
- The Endothelial Glycocalyx as a Target of Excess Soluble Fms-like Tyrosine Kinase-1.International journal of molecular sciences · 2023Article
- ADAM10-a "multitasker" in sepsis: focus on its posttranslational target.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- The Endothelial Glycocalyx and Neonatal Sepsis.International journal of molecular sciences · 2022Review
- The Role of IGL-2 Preservation Solution on Rat Livers during SCS and HOPE.International journal of molecular sciences · 2022Article
- Endothelial Glycocalyx Degradation in Critical Illness and Injury.Frontiers in medicine · 2022Review
- Endothelial glycocalyx in hepatopulmonary syndrome: An indispensable player mediating vascular changes.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Leukocyte adhesion to the endothelium is an important early step in the initiation and progression of sepsis. The endothelial glycocalyx layer (EGL) has been implicated in neutrophil adhesion and barrier dysfunction, but studies in this area are few. In this report, we examine the hypothesis that damage to the structure of the EGL caused by inflammation leads to increased leukocyte adhesion and endothelial barrier dysfunction. We used human umbilical vein endothelial cells enzymatically treated to remove the EGL components hyaluronic acid (HA) and heparan sulfate (HS) as a model for EGL damage. Using atomic force microscopy, we show reductions in EGL thickness after removal of either HA or HS individually, but the largest decrease, comparable with TNF-α treatment, was observed when both HA and HS were removed. Interestingly, removal of HS or HA individually did not affect neutrophil adhesion significantly, but removal of both constituents resulted in increased neutrophil adhesion. To test EGL contributions to endothelial barrier properties, we measured transendothelial electrical resistance (TEER) and diffusion of fluorescently labeled dextran (10 kDa molecular weight) across the monolayer. Removal of EGL components decreased TEER but had an insignificant effect on dextran diffusion rates. The reduction in TEER suggests that disruption of the EGL may predispose endothelial cells to increased rates of fluid leakage. These data support the view that damage to the EGL during inflammation has significant effects on the accessibility of adhesion molecules, likely facilitates leukocyte adhesion, and may also contribute to increased rates of fluid transport into tissues.
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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.