ArticleMolecular and cellular biochemistry2014
Novel mechanism regulating endothelial permeability via T-cadherin-dependent VE-cadherin phosphorylation and clathrin-mediated endocytosis.
Article in Molecular and cellular biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- T‑cadherin and its impact on human diseases (Review).Molecular medicine reports · 2026Review
- T-cadherin as a potential novel regulator of intestinal inflammation and fibrosis.Frontiers in physiology · 2026Review
- T-Cadherin Finetunes Proliferation-Differentiation During Adipogenesis via PI3K-AKT Signaling Pathway.International journal of molecular sciences · 2025Article
- Decoding the enigmatic role of T-cadherin in tumor angiogenesis.Frontiers in immunology · 2025Review
- New evidence for T-cadherin in COVID-19 pathogenesis, endothelial dysfunction, and lung fibrosis.Frontiers in cell and developmental biology · 2025Article
- Alveolar-capillary endocytosis and trafficking in acute lung injury and acute respiratory distress syndrome.Frontiers in immunology · 2024Review
- VE-Cadherin and Vesicles Differentially Regulate Lymphatic Vascular Permeability to Solutes of Various Sizes.Frontiers in physiology · 2021Article
- Oxygen-Glucose Deprivation/Reoxygenation Induces Human Brain Microvascular Endothelial Cell Hyperpermeability Via VE-Cadherin Internalization: Roles of RhoA/ROCK2.Journal of molecular neuroscience : MN · 2019Article
- Effect of adiponectin level and genetic variation of its receptors on diabetic retinopathy: A case-control study.Medicine · 2019Article
- Desacetylvinblastine Monohydrazide Disrupts Tumor Vessels by Promoting VE-cadherin Internalization.Theranostics · 2018Article
- The Role of IL-33 on LPS-Induced Acute Lung Injury in Mice.Inflammation · 2017Article
- T-cadherin deficiency increases vascular vulnerability in T2DM through impaired NO bioactivity.Cardiovascular diabetology · 2017Article
- Inhibitory effects of pigment epithelium-derived factor on epithelial-mesenchymal transition, migration and invasion of breast cancer.International journal of clinical and experimental pathology · 2017Article
- The VE-cadherin cytoplasmic domain undergoes proteolytic processing during endocytosis.Molecular biology of the cell · 2017Article
- Cytokine-Ion Channel Interactions in Pulmonary Inflammation.Frontiers in immunology · 2017Review
- Pharmacoproteomic analysis reveals that metapristone (RU486 metabolite) intervenes E-cadherin and vimentin to realize cancer metastasis chemoprevention.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
T-cadherin is a unique member of the cadherin superfamily of adhesion molecules. In contrast to "classical" cadherins, T-cadherin lacks transmembrane and cytoplasmic domains and is anchored to the cell membrane via a glycosilphosphoinositol moiety. T-cadherin is predominantly expressed in cardiovascular system. Clinical and biochemical studies evidence that expression of T-cadherin increases in post-angioplasty restenosis and atherosclerotic lesions-conditions associated with endothelial dysfunction and pathological expression of adhesion molecules. Here, we provide data suggesting a new signaling mechanism by which T-cadherin regulates endothelial permeability. T-cadherin overexpression leads to VE-cadherin phosphorylation on Y731 (β-catenin-binding site), VE-cadherin clathrin-dependent endocytosis and its degradation in lysosomes. Moreover, T-cadherin overexpression results in activation of Rho GTPases signaling and actin stress fiber formation. Thus, T-cadherin up-regulation is involved in degradation of a key endothelial adhesion molecule, VE-cadherin, resulting in the disruption of endothelial barrier function. Our results point to the role of T-cadherin in regulation of endothelial permeability and its possible engagement in endothelial dysfunction.
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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.