ArticleEMBO reports2024
Ubiquitination of VE-cadherin regulates inflammation-induced vascular permeability in vivo.
Article in EMBO reports, 2024. 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.
- tVNS Mitigates Neuroinflammation and Nociception in a Rodent LPS Endotoxemia Model.Clinical and translational science · 2026Article
- PCSK9 orchestrates the antigen presentation-endothelial barrier axis to potentiate immune exclusion in colorectal cancer.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- VE-cadherin interaction proteomics identifies ARVCF as stabilizer of endothelial adherens junctions.iScience · 2026Article
- Plakoglobin transmits tension across VE-cadherin for vascular leak formation and leukocyte diapedesis.The EMBO journal · 2026Article
- SHP2 regulates VEGFR2 Y1175/PLCγ signaling to impair tumor endothelial barrier stability.iScience · 2026Article
- Hypoxia-Driven Pulmonary Adaptation in the Yak: A Homeostatic Mechanism Mediated by Cell Adhesion Molecules.International journal of molecular sciences · 2026Article
- Targeted 2-Deoxy-D-Ribose Delivery by Biomimetic Nanoplatform Activates EGFR for Accelerated Heart Valve Endothelialization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Pentadecanoic acid (C15:0) and cardiovascular disease: A narrative review.World journal of cardiology · 2025Review
- Acinar-derived VEGF-A orchestrates blood vascular remodeling and preserves microvessels during acute pancreatitis.Cell communication and signaling : CCS · 2025Article
- Engineered immune-driven theranostics for clinical cardiology.Military Medical Research · 2025Review
- Rab7a is required to degrade select blood-brain barrier junctional proteins after ischemic stroke.Acta neuropathologica communications · 2025Article
- Distinct VE-cadherin serine and tyrosine phosphorylation sites and their role for inflammation-induced vascular permeability in vivo.Cellular and molecular life sciences : CMLS · 2025Article
- A dual-targeting bio-liposomes nanodrug repair endothelial cell dysfunction and restore macrophage cholesterol flow homeostasis to treat early atherosclerosis.Journal of nanobiotechnology · 2025Article
- Recent advances in surface functionalization of cardiovascular stents.Bioactive materials · 2025Review
- VE-PTP controls a fluid shear stress set point that governs cell morphological responses through Tie-2.Frontiers in cell and developmental biology · 2025Article
- Article
- Tie-2 regulates endothelial morphological responses to shear stress by FOXO1-triggered autophagy.PloS one · 2025Article
- VE-cadherin RGD motifs are dispensable for cell-cell junctions, endothelial barrier function and monocyte extravasation.Tissue barriers · 2025Article
- Csk controls leukocyte extravasation via local regulation of Src family kinases and cortactin signaling.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
VE-cadherin is a major component of the cell adhesion machinery which provides integrity and plasticity of the barrier function of endothelial junctions. Here, we analyze whether ubiquitination of VE-cadherin is involved in the regulation of the endothelial barrier in inflammation in vivo. We show that histamine and thrombin stimulate ubiquitination of VE-cadherin in HUVEC, which is completely blocked if the two lysine residues K626 and K633 are replaced by arginine. Similarly, these mutations block histamine-induced endocytosis of VE-cadherin. We describe two knock-in mouse lines with endogenous VE-cadherin being replaced by either a VE-cadherin K626/633R or a VE-cadherin KallR mutant, where all seven lysine residues are mutated. Mutant mice are viable, healthy and fertile with normal expression levels of junctional VE-cadherin. Histamine- or LPS-induced vascular permeability in the skin or lung of both of these mutant mice are clearly and similarly reduced in comparison to WT mice. Additionally, we detect a role of K626/633 for lysosomal targeting. Collectively, our findings identify ubiquitination of VE-cadherin as important for the induction of vascular permeability in the inflamed skin and lung.
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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.