ArticleMolecular biology of the cell2017
Regulation of endothelial barrier function by p120-catenin∙VE-cadherin interaction.
Article in Molecular biology of the cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- The interplay of integrin, VE-cadherin, and β-catenin signaling triad in angiogenesis: regulation by Wnt antagonist, secreted frizzled related protein 4 in the tumor angiogenic loop.Medical oncology (Northwood, London, England) · 2026Review
- VE-cadherin interaction proteomics identifies ARVCF as stabilizer of endothelial adherens junctions.iScience · 2026Article
- Inhibition of junctional protein disruption by 2,4,6-trihydroxy-3-geranyl acetophenone in lipopolysaccharide-induced endothelial hyperpermeability via GEF-H1/RhoA/ROCK pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- FYN regulates aqueous humor outflow and IOP through the phosphorylation of VE-CADHERIN.Nature communications · 2025Article
- Slit2-Robo4 signal pathway and tight junction in intestine mediate LPS-induced inflammation in mice.European journal of medical research · 2024Article
- Essential role of obscurin kinase-1 in cardiomyocyte coupling via N-cadherin phosphorylation.JCI insight · 2024Article
- Alveolar-capillary endocytosis and trafficking in acute lung injury and acute respiratory distress syndrome.Frontiers in immunology · 2024Review
- The Role of Txnip in Mediating Low-Magnesium-Driven Endothelial Dysfunction.International journal of molecular sciences · 2023Article
- Engineered Vasculogenic Extracellular Vesicles Drive Nonviral Direct Conversions of Human Dermal Fibroblasts into Induced Endothelial Cells and Improve Wound Closure.Advanced therapeutics · 2023Article
- Tauroursodeoxycholic Acid Alleviates Endoplasmic Reticulum Stress-Mediated Visual Deficits in Diabetic tie2-TNF Transgenic Mice via TGR5 Signaling.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2023Article
- Trafficking in blood vessel development.Angiogenesis · 2022Review
- Heterologous production of the adhesin LIC13411 from pathogenicFrontiers in cellular and infection microbiology · 2022Article
- Small Extracellular Vesicles Propagate the Inflammatory Response After Trauma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Effects of nicorandil on p120 expression in the spinal cord and dorsal root ganglion of rats with chronic postsurgical pain.Molecular medicine reports · 2020Article
- Article
- α1AMP-Activated Protein Kinase Protects against Lipopolysaccharide-Induced Endothelial Barrier Disruption via Junctional Reinforcement and Activation of the p38 MAPK/HSP27 Pathway.International journal of molecular sciences · 2020Article
- Advances in mammalian target of rapamycin kinase inhibitors: application to devices used in the treatment of coronary artery disease.Future medicinal chemistry · 2020Review
- VE-cadherin endocytosis controls vascular integrity and patterning during development.The Journal of cell biology · 2020Article
- Vascular permeability in retinopathy is regulated by VEGFR2 Y949 signaling to VE-cadherin.eLife · 2020Article
- GRP78 translocation to the cell surface and O-GlcNAcylation of VE-Cadherin contribute to ER stress-mediated endothelial permeability.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Endothelial p120-catenin (p120) maintains the level of vascular endothelial cadherin (VE-Cad) by inhibiting VE-Cad endocytosis. Loss of p120 results in a decrease in VE-Cad levels, leading to the formation of monolayers with decreased barrier function (as assessed by transendothelial electrical resistance [TEER]), whereas overexpression of p120 increases VE-Cad levels and promotes a more restrictive monolayer. To test whether reduced endocytosis mediated by p120 is required for VE-Cad formation of a restrictive barrier, we restored VE-Cad levels using an endocytic-defective VE-Cad mutant. This endocytic-defective mutant was unable to rescue the loss of TEER associated with p120 or VE-Cad depletion. In contrast, the endocytic-defective mutant was able to prevent sprout formation in a fibrin bead assay, suggesting that p120•VE-Cad interaction regulates barrier function and angiogenic sprouting through different mechanisms. Further investigation found that depletion of p120 increases Src activity and that loss of p120 binding results in increased VE-Cad phosphorylation. In addition, expression of a Y658F-VE-Cad mutant or an endocytic-defective Y658F-VE-Cad double mutant were both able to rescue TEER independently of p120 binding. Our results show that in addition to regulating endocytosis, p120 also allows the phosphorylated form of VE-Cad to participate in the formation of a restrictive monolayer.
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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.