ArticleMolecular biology of the cell2014
ARP2/3-mediated junction-associated lamellipodia control VE-cadherin-based cell junction dynamics and maintain monolayer integrity.
Article in Molecular biology of the cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
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Who cites it
87 citing papers in PubMed, 138 citations in OpenAlex.
- NCKAP1 coordinates focal adhesion and adherens junction dynamics in endothelial barrier maintenance and angiogenesis.iScience · 2026Article
- VE-Cadherin-Actin Regulation Promotes Mechanotransduction and Monolayer Maturation Involving a Tension-Sensitive Intermediate State.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- High-Altitude Hypoxic Preconditioning Attenuates Lipopolysaccharide-Induced Lung Injury and is Associated with Alveolar-Capillary Barrier Maintenance.Journal of inflammation research · 2026Article
- Endocytic Pathways and Actin Remodeling Mediate Everolimus-Induced VE-Cadherin Disorganization and Barrier Dysfunction.Cellular and molecular bioengineering · 2025Article
- Endothelial-smooth muscle microgauges for modeling pulmonary arterial vasoregulation.Lab on a chip · 2025Article
- The Duality of Collagens in Metastases of Solid Tumors.International journal of molecular sciences · 2025Review
- Please inhibit responsibly: Natural and synthetic actin toxins as useful tools in cell biology.Molecular biology of the cell · 2025Review
- A systematic investigation of endothelial cell behavior under hydrostatic pressure.Scientific reports · 2025Article
- Elevated hydrostatic pressure destabilizes VE-cadherin junctions in a time and shear stress dependent manner: An endothelium-on-chip study.APL bioengineering · 2025Article
- Plexin/Semaphorin antagonism orchestrates collective cell migration and organ sculpting by regulating epithelial-mesenchymal balance.Science advances · 2025Article
- A specific role for endothelial EPLIN-isoform-regulated actin dynamics in neutrophil transmigration.Scientific reports · 2025Article
- Formation of tight junction-like structures of zonula occludens 2 in platelet-platelet interaction.Research and practice in thrombosis and haemostasis · 2025Article
- The role of actin cytoskeleton component Arp2/3 in inflammatory response.Frontiers in cell and developmental biology · 2025Review
- TNF-α induces VE-cadherin-dependent gap/JAIL cycling through an intermediate state essential for neutrophil transmigration.Frontiers in immunology · 2025Article
- Junctions at the crossroads: the impact of mechanical cues on endothelial cell-cell junction conformations and vascular permeability.American journal of physiology. Cell physiology · 2024Review
- Article
- Helical vasculogenesis driven by cell chirality.Science advances · 2024Article
- Role of cell rearrangement and related signaling pathways in the dynamic process of tip cell selection.Cell communication and signaling : CCS · 2024Review
- Imaging and Analysis of the Dynamics of Filamentous Actin Structures in Live Endothelial Cells.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Magneto-Mechanical Actuation Induces Endothelial Permeability.ACS biomaterials science & engineering · 2023Article
27 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Maintenance and remodeling of endothelial cell junctions critically depend on the VE-cadherin/catenin complex and its interaction with the actin filament cytoskeleton. Here we demonstrate that local lack of vascular endothelial (VE)-cadherin at established cell junctions causes actin-driven and actin-related protein 2/3 complex (ARP2/3)-controlled lamellipodia to appear intermittently at those sites. Lamellipodia overlap the VE-cadherin-free adjacent plasma membranes and facilitate formation of new VE-cadherin adhesion sites, which quickly move into the junctions, driving VE-cadherin dynamics and remodeling. Inhibition of the ARP2/3 complex by expression of the N-WASP (V)CA domain or application of two ARP2/3 inhibitors, CK-548 and CK-666, blocks VE-cadherin dynamics and causes intercellular gaps. Furthermore, expression of carboxy-terminal-truncated VE-cadherin increases the number of ARP2/3-controlled lamellipodia, whereas overexpression of wild-type VE-cadherin largely blocks it and decreases cell motility. The data demonstrate a functional interrelationship between VE-cadherin-mediated cell adhesion and actin-driven, ARP2/3-controlled formation of new VE-cadherin adhesion sites via intermittently appearing lamellipodia at established cell junctions. This coordinated mechanism controls VE-cadherin dynamics and cell motility and maintains monolayer integrity, thus potentially being relevant in disease and angiogenesis.
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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.