ArticlePloS one2014
Different contributions of clathrin- and caveolae-mediated endocytosis of vascular endothelial cadherin to lipopolysaccharide-induced vascular hyperpermeability.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- MMP8 exacerbates sepsis-induced pulmonary vascular leakage by disruption of endothelial VE-cadherin through ERK signalling.Molecular biomedicine · 2026Article
- Extracellular RNAs as Messengers and Early Biomarkers in Neurodegeneration.International journal of molecular sciences · 2025Review
- Endocytic Pathways and Actin Remodeling Mediate Everolimus-Induced VE-Cadherin Disorganization and Barrier Dysfunction.Cellular and molecular bioengineering · 2025Article
- Exploring the Mechanisms Underlying Cellular Uptake and Activation of Dendritic Cells by the GK-1 Peptide.ACS omega · 2024Article
- Review
- Ultrastructural Remodeling of the Blood-Brain Barrier and Neurovascular Unit by Lipopolysaccharide-Induced Neuroinflammation.International journal of molecular sciences · 2023Article
- Advances in oral peptide drug nanoparticles for diabetes mellitus treatment.Bioactive materials · 2022Review
- Blood-Brain Barrier Mechanisms in Stroke and Trauma.Handbook of experimental pharmacology · 2022Review
- Suppressive effects of quercetin on hydrogen peroxide-induced caveolin-1 phosphorylation in endothelial cells.Journal of clinical biochemistry and nutrition · 2021Article
- Physical and mechanical cues affecting biomaterial-mediated plasmid DNA delivery: insights into non-viral delivery systems.Journal, genetic engineering & biotechnology · 2021Review
- Charge-switchable zwitterionic polycarboxybetaine particle as an intestinal permeation enhancer for efficient oral insulin delivery.Theranostics · 2021Article
- Simvastatin ameliorates oxygen glucose deprivation/reoxygenation-induced pulmonary endothelial barrier dysfunction by restoring cell-cell junctions and actin cytoskeleton dynamics via the PI3K/Akt signaling pathway.American journal of translational research · 2020Article
- Different concentrations of lipopolysaccharide regulate barrier function through the PI3K/Akt signalling pathway in human pulmonary microvascular endothelial cells.Scientific reports · 2018Article
- Transmission of α-synuclein-containing erythrocyte-derived extracellular vesicles across the blood-brain barrier via adsorptive mediated transcytosis: another mechanism for initiation and progression of Parkinson's disease?Acta neuropathologica communications · 2017Article
- The VE-cadherin cytoplasmic domain undergoes proteolytic processing during endocytosis.Molecular biology of the cell · 2017Article
- A Comparative Study on the Alterations of Endocytic Pathways in Multiple Lysosomal Storage Disorders.Molecular pharmaceutics · 2016Article
- The role of sphingolipids in endothelial barrier function.Biological chemistry · 2015Review
- Control of vascular permeability by adhesion molecules.Tissue barriers · 2015Article
- Ulinastatin inhibits oxidant-induced endothelial hyperpermeability and apoptotic signaling.International journal of clinical and experimental pathology · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular hyperpermeability induced by lipopolysaccharide (LPS) is a common pathogenic process in cases of severe trauma and sepsis. Vascular endothelial cadherin (VE-cad) is a key regulatory molecule involved in this process, although the detailed mechanism through which this molecule acts remains unclear. We assessed the role of clathrin-mediated and caveolae-mediated endocytosis of VE-cad in LPS-induced vascular hyperpermeability in the human vascular endothelial cell line CRL-2922 and determined that vascular permeability and VE-cad localization at the plasma membrane were negatively correlated after LPS treatment. Additionally, the loss of VE-cad at the plasma membrane was caused by both clathrin-mediated and caveolae-mediated endocytosis. Clathrin-mediated endocytosis was dominant early after LPS treatment, and caveolae-mediated endocytosis was dominant hours after LPS treatment. The caveolae-mediated endocytosis of VE-cad was activated through the LPS-Toll-like receptor 4 (TLR4)-Src signaling pathway. Structural changes in the actin cytoskeleton, specifically from polymerization to depolymerization, were important reasons for the switching of the VE-cad endocytosis pathway from clathrin-mediated to caveolae-mediated. Our findings suggest that clathrin-mediated and caveolae-mediated endocytosis of VE-cad contribute to LPS-induced vascular hyperpermeability, although they contribute via different mechanism. The predominant means of endocytosis depends on the time since LPS treatment.
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