ArticleThe American journal of pathology2006
PECAM-1 affects GSK-3beta-mediated beta-catenin phosphorylation and degradation.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 72 citations in OpenAlex.
- Endothelial transdifferentiation of glioma stem cells: a literature review.Acta neuropathologica communications · 2025Review
- Unraveling the Role of the Wnt Pathway in Hepatocellular Carcinoma: From Molecular Mechanisms to Therapeutic Implications.Journal of clinical and translational hepatology · 2025Review
- Plakoglobin does not participate in endothelial barrier stabilization mediated by cAMP.Scientific reports · 2025Article
- Low or oscillatory shear stress and endothelial permeability in atherosclerosis.Frontiers in physiology · 2024Review
- Endothelial mechanobiology in atherosclerosis.Cardiovascular research · 2023Review
- CD31 as a probable responding and gate-keeping protein of the blood-brain barrier and the risk of Alzheimer's disease.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Review
- Disturbed flow increases endothelial inflammation and permeability via a Frizzled-4-β-catenin-dependent pathway.Journal of cell science · 2023Article
- Review
- SARS-CoV-2 Spike Protein Induces Degradation of Junctional Proteins That Maintain Endothelial Barrier Integrity.Frontiers in cardiovascular medicine · 2021Article
- Src Homology 2 Domain-Containing Protein Tyrosine Phosphatase Promotes Inflammation and Accelerates Osteoarthritis by Activating β-Catenin.Frontiers in cell and developmental biology · 2021Article
- Preservation of microvascular barrier function requires CD31 receptor-induced metabolic reprogramming.Nature communications · 2020Article
- The blood-brain barrier in health and disease: Important unanswered questions.The Journal of experimental medicine · 2020Review
- Hyperglycemia-induced ubiquitination and degradation of β-catenin with the loss of platelet endothelial cell adhesion molecule-1 in retinal endothelial cells.Microcirculation (New York, N.Y. : 1994) · 2020Article
- Endothelial responses to shear stress in atherosclerosis: a novel role for developmental genes.Nature reviews. Cardiology · 2020Review
- Loss of Platelet Endothelial Cell Adhesion Molecule-1 (PECAM-1) in the Diabetic Retina: Role of Matrix Metalloproteinases.Investigative ophthalmology & visual science · 2019Article
- PECAM-1 Stabilizes Blood-Brain Barrier Integrity and Favors Paracellular T-Cell Diapedesis Across the Blood-Brain Barrier During Neuroinflammation.Frontiers in immunology · 2019Article
- Effects of cigarette smoke on pulmonary endothelial cells.American journal of physiology. Lung cellular and molecular physiology · 2018Review
- CRISPR-mediated deletion of the PECAM-1 cytoplasmic domain increases receptor lateral mobility and strengthens endothelial cell junctional integrity.Life sciences · 2018Article
- Bone marrow-derived mesenchymal stem cells alleviates renal injury in severe acute pancreatitis via RhoA/Rho kinase.International journal of clinical and experimental pathology · 2017Article
- The CD31 molecule: a possible neuroprotective agent in acute ischemic stroke?Thrombosis journal · 2017Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) regulates a variety of endothelial and immune cell biological responses. PECAM-1-null mice exhibit prolonged and increased permeability after inflammatory insults. We observed that in PECAM-1-null endothelial cells (ECs), beta-catenin remained tyrosine phosphorylated, coinciding with a sustained increase in permeability. Src homology 2 domain containing phosphatase 2 (SHP-2) association with beta-catenin was diminished in PECAM-1-null ECs, suggesting that lack of PECAM-1 inhibits the ability of this adherens junction component to become dephosphorylated, promoting a sustained increase in permeability. beta-Catenin/Glycogen synthase kinase 3 (GSK-3beta) association and beta-catenin serine phosphorylation levels were increased and beta-catenin expression levels were reduced in PECAM-1-null ECs. Glycogen synthase kinase 3 (GSK-3beta) serine phosphorylation (inactivation) was blunted in PECAM-1-null ECs after histamine treatment or shear stress. Our data suggest that PECAM-1 serves as a critical dynamic regulator of endothelial barrier permeability. On stimulation by a vasoactive substance or shear stress, PECAM-1 became tyrosine phosphorylated, enabling recruitment of SHP-2 and tyrosine-phosphorylated beta-catenin to its cytoplasmic domain, facilitating dephosphorylation of beta-catenin, and allowing reconstitution of adherens junctions. In addition, PECAM-1 modulated the levels of beta-catenin by regulating the activity of GSK-3beta, which in turn affected the serine phosphorylation of beta-catenin and its proteosomal degradation, affecting the ability of the cell to reform adherens junctions in a timely fashion.
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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.