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proportional cellular responses to maintain the endothelial barrier ( 10 ). VE–cadherin-based adherens junctions (AJs) are crucial adhesion structures that form endothelial cell–cell contacts ( 11 , 12 ). Endothelial junction remodelling is required for
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in the endothelial barrier, however, means that the process must be tightly controlled. ECs are connected to each other by adherens junctions and tight junctions to form a barrier that excludes all but small molecules ( 4 ). The organization of these
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Department of Medical Specializations – Cardiology, University of Geneva, Geneva, Switzerland
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Department of Medical Specializations – Cardiology, University of Geneva, Geneva, Switzerland
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intercellular space and adherens junctions (AJs) providing mechanical anchorage ( 36 ), recent evidence suggests that GJs and/or Cxs may play a role in the regulation of the endothelial barrier function as well ( 37 ). Cx40 is abundantly expressed in the lung
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Leeuwenhoek Centre for Advanced Microscopy, Section Molecular Cytology at Swammerdam Institute for Life Sciences at University of Amsterdam, Amsterdam, the Netherlands
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signalling can induce tyrosine phosphorylation of VE-cadherin at Tyr658 and Tyr731 via the activation of two tyrosine kinases, Src and Pyk2 ( 49 ). VE-cadherin is a major constituent of adherens junctions and connects ECs by binding to the actin cytoskeleton
Instituto Superior Técnico, Universidade de Lisboa, Lisboa, Portugal
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Instituto de Histologia e Biologia do Desenvolvimento, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal
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. Phosphorylated FOXO1 will enter the EC tip nuclei and promote transcription of polarity and migration-related genes. YAP/TAZ transcription factors are crucial for the activation of CDC42 and for adherens junction’s integrity and stabilization. WNT5A/ROR2
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by the presence of not only adherens junctions (AJs) but also a molecularly unique and complex as well as continuous network of TJs ( 12 ). The transmembrane vascular endothelial cadherin (VE-cadherin) mediates homophilic adhesion at the level of BBB
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have demonstrated the importance of direct EC–pericyte contact for cell–cell communication through physical interactions, including gap junctions, such as connexin 43 ( 13 ), and adherens junctions, specifically N-cadherin ( 14 ). However, constructing
Leeuwenhoek Centre for Advanced Microscopy, Section Molecular Cytology at Swammerdam Institute for Life Sciences, the University of Amsterdam, Amsterdam, the Netherlands
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Department of Molecular Hematology, Sanquin Research, and Landsteiner Laboratory, Molecular Cell Biology Lab, Amsterdam, the Netherlands
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Leeuwenhoek Centre for Advanced Microscopy, Section Molecular Cytology at Swammerdam Institute for Life Sciences, the University of Amsterdam, Amsterdam, the Netherlands
Department of Molecular Hematology, Sanquin Research, and Landsteiner Laboratory, Molecular Cell Biology Lab, Amsterdam, the Netherlands
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morphological defects on our monolayers that were depleted for ICAM2 in our phase-contrast images. We did not study junctional phenotype via immunofluorescent stains of adherens junctions (e.g. VE-cadherin) or tight junction (e.g. claudin 5) proteins, but based
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adherens junction molecules such as vascular endothelial (VE)-cadherin ( 24 ). In addition, endothelial cells of a normalised vasculature are supported by higher numbers of pericytes or pericytes which are more mature and adhesive ( 13 , 20 , 22 ). While
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Department of Mechanical Engineering, Temple University, Philadelphia, Pennsylvania, USA
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-receptor interaction, WnT signaling, metabolism Tmem100, Scn7a, Adrb1, Daam1, Nkd1 MG JAK-STAT, NOD-like receptor signaling, MAPK signaling Emp1 Atf4, Dusp5, Gadd45b, Myc, Relb Pancreas Adherens junction, focal adhesion, MAPK
