Review
Physiology
Weijin Nan, Yuxi He, Shurong Wang, Yan Zhang
Summary: VE-cadherin is an endothelium-specific adhesion protein found in the junctions between endothelial cells. It is crucial for maintaining the homogeneity of endothelial cells and plays important roles in vascular development, permeability, and tumor angiogenesis.
FRONTIERS IN PHYSIOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Nida Arif, Maren Zinnhardt, Alengo Nyamay'Antu, Denise Teber, Randy Brueckner, Kerstin Schaefer, Yu-Tung Li, Britta Trappmann, Carsten Grashoff, Dietmar Vestweber
Summary: The study reveals the mechanism of leukocyte extravasation during the immune response, which involves the destabilization of endothelial junctions through PECAM-1-SHP2-triggered dephosphorylation of VE-cadherin-Y731. This process requires various biochemical and biomechanical factors, such as Ca2+ signaling, non-muscle myosin II activation, and endothelial cell tension.
Article
Multidisciplinary Sciences
Rina Hashimoto, Junya Takahashi, Keisuke Shirakura, Risa Funatsu, Kaori Kosugi, Sayaka Deguchi, Masaki Yamamoto, Yugo Tsunoda, Maaya Morita, Kosuke Muraoka, Masato Tanaka, Tomoaki Kanbara, Shota Tanaka, Shigeyuki Tamiya, Nagisa Tokunoh, Atsushi Kawai, Masahito Ikawa, Chikako Ono, Keisuke Tachibana, Masuo Kondoh, Masanori Obana, Yoshiharu Matsuura, Akihiro Ohsumi, Takeshi Noda, Takuya Yamamoto, Yasuo Yoshioka, Yu-Suke Torisawa, Hiroshi Date, Yasushi Fujio, Miki Nagao, Kazuo Takayama, Yoshiaki Okada
Summary: This study found that SARS-CoV-2 decreases the expression of Claudin-5 (CLDN5), a tight junction protein, and disrupts vascular endothelial cadherin-mediated adherens junctions, thereby leading to the disruption of the endothelial barrier in respiratory organs. The down-regulation of CLDN5 expression was observed in the lungs of a COVID-19 patient. The overexpression of CLDN5 or treatment with Fluvastatin rescued the SARS-CoV-2-induced respiratory endothelial barrier disruption. Inducing CLDN5 expression is identified as a therapeutic strategy against COVID-19.
Article
Cell & Tissue Engineering
Violetta A. Maltabe, Anna N. Melidoni, Dimitris Beis, Ioannis Kokkinopoulos, Nikolaos Paschalidis, Panos Kouklis
Summary: The study found that ISL1+ cardiovascular progenitor cells form adherens junctions through VE-CADHERIN during differentiation, which is crucial for cardiac differentiation.
Article
Biochemistry & Molecular Biology
Roberta Lugano, Kalyani Vemuri, Stefano Barbera, Maurizio Orlandini, Elisabetta Dejana, Lena Claesson-Welsh, Anna Dimberg
Summary: CD93 regulates the stability of VE-cadherin at endothelial junctions by interacting with VE-cadherin and limiting its phosphorylation and turnover. CD93 deficiency leads to increased phosphorylation of VE-cadherin, displacing it from endothelial cell-cell contacts and disrupting endothelial junctions, resulting in enhanced blood-brain barrier permeability. This mechanism is regulated through the Rho/Rho kinase-dependent pathway.
Article
Multidisciplinary Sciences
Caterina Ivaldo, Mario Passalacqua, Anna Lisa Furfaro, Cristina d'Abramo, Santiago Ruiz, Prodyot K. Chatterjee, Christine N. Metz, Mariapaola Nitti, Philippe Marambaud
Summary: Oxidative stress induced efficient proteolysis of VE-cadherin by MMPs and gamma-secretase in HUVECs. The cytoplasmic domain of VE-cadherin produced by gamma-secretase, VE-Cad/CTF2, was tightly regulated and sequentially produced from an ADAM10/17-generated C-terminal fragment. BMP9 and BMP10 reduced VE-Cad/CTF2 levels and mitigated H2O2-mediated actin cytoskeleton disassembly.
SCIENTIFIC REPORTS
(2023)
Article
Cardiac & Cardiovascular Systems
Ki-Sook Park, Leslayann Schecterson, Barry M. Gumbiner
Summary: The study identified monoclonal antibodies that can activate cell adhesion, inhibit increased endothelial permeability induced by various signaling factors, and stabilize cell junctions, suggesting potential therapeutic implications for treating vascular leakiness and inflammation.
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Typhaine Anquetil, Romain Solinhac, Aude Jaffre, Gaetan Chicanne, Julien Viaud, Jean Darcourt, Cyrille Orset, Eva Geuss, Christoph Kleinschnitz, Bart Vanhaesebroeck, Denis Vivien, Karim Hnia, Vincent Larrue, Bernard Payrastre, Marie-Pierre Gratacap
Summary: Protecting endothelial cells is critical in preventing the impact of vascular leakage and edema on pathological conditions. PI3KC2 beta could be a potential new therapeutic target for treating aggravating lesions following ischemic stroke.
Article
Cell Biology
Cao Nguyen Duong, Randy Brueckner, Martina Schmitt, Astrid F. Nottebaum, Laura J. Braun, Marika Meyer Zu Brickwedde, Ute Ipe, Hermann Vom Bruch, Hans R. Schoeler, Giuseppe Trapani, Britta Trappmann, Mirsana P. Ebrahimkutty, Stephan Huveneers, Johan de Rooij, Noboru Ishiyama, Mitsuhiko Ikura, Dietmar Vestweber
Summary: Cadherin-mediated cell adhesion relies on anchoring to the actin cytoskeleton via the beta-catenin-alpha-catenin complex. Fusion of VE-cadherin to alpha-catenin enhances this anchorage in endothelial cells, leading to stabilized endothelial junctions. The mechanism involves constitutive recruitment of vinculin by VE-cadherin-alpha-catenin, as well as conformational changes in the actin-binding domain of alpha-catenin.
JOURNAL OF CELL SCIENCE
(2021)
Article
Biochemistry & Molecular Biology
Jay Rollins, Tyler Worthington, Allison Dransfield, Jordan Whitney, Jordan Stanford, Emily Hooke, Joseph Hobson, Jacob Wengler, Sandra Hope, Dario Mizrachi
Summary: Cell-adhesion molecules (CAMs) are responsible for various cell interactions. In this study, the expression of CLDN proteins in E. coli is investigated and its consequences are discussed. The iCLASP method is introduced as a high-throughput screening approach for identifying paracellular modulators for CLDN2.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Medicine, Research & Experimental
Keisuke Shirakura, Peter Baluk, Astrid F. Nottebaum, Ute Ipe, Kevin G. Peters, Donald M. McDonald, Dietmar Vestweber
Summary: Vascular endothelial protein tyrosine phosphatase (VE-PTP) affects endothelial barrier function by regulating Tie2 activation. High shear stress caused VE-PTP polarization and endocytosis, along with Tie2 activation, in regions with smooth flow. In regions with disturbed flow, VE-PTP remained associated with Tie2. Endothelial cells exposed to high shear stress had increased Tie2 activation and reduced macromolecular permeability. Deleting VE-PTP or inhibiting it with AKB-9785 had similar anti-atherogenic effects.
EMBO MOLECULAR MEDICINE
(2023)
Review
Biochemistry & Molecular Biology
Daniel Delgado-Bellido, F. J. Oliver, Maria Victoria Vargas Padilla, Laura Lobo-Selma, Antonio Chacon-Barrado, Juan Diaz-Martin, Enrique de alava
Summary: Tumor growth can be facilitated by the expansion of blood vessels or the development of vasculogenic mimicry (VM), a novel pathway involving aggressive tumor cells expressing endothelial cell markers. VM is associated with high tumor grade, cancer cell invasion, metastasis, and reduced survival. This review summarizes studies on angiogenesis and aberrant angiogenesis by tumor cells, discusses the intracellular signaling mechanisms involved in VM formation, and explores the implications for tumor angiogenesis and targeted therapy.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Medicine, General & Internal
Shiyue Wang, Xin Li, Han Jiang, Jian Zhang
Summary: In this study, the diagnostic value of serum VEC and Vcn for TBAD was evaluated. The results showed that the concentrations of VEC and Vcn were significantly higher in TBAD patients compared to healthy controls. Combined detection of VEC and Vcn improved the accuracy of TBAD diagnosis. High serum Vcn concentration was associated with increased risk of visceral malperfusion in TBAD patients. Therefore, VEC and Vcn have the potential to be serum markers for TBAD.
JOURNAL OF CLINICAL MEDICINE
(2023)
Article
Otorhinolaryngology
Nitish Khurana, Abigail Pulsipher, Jolanta Jedrzkiewicz, Shaelene Ashby, Chelsea E. Pollard, Hamidreza Ghandehari, Jeremiah A. Alt
Summary: Significant increases in vascularity, pro-angiogenic gene and protein expression, as well as blood vessel morphogenesis, were observed in CRS patients compared with controls. In addition, the fenestration sizes between interendothelial junction structures were larger in CRS patients than in controls, suggesting inflammation-driven vascular dysregulation in CRS pathology.
INTERNATIONAL FORUM OF ALLERGY & RHINOLOGY
(2021)
Article
Oncology
Xiaocui Chen, Shuqiong Zhang, Kun Du, Naisheng Zheng, Yi Liu, Hui Chen, Guohua Xie, Yanhui Ma, Yunlan Zhou, Yingxia Zheng, Lingfang Zeng, Junyao Yang, Lisong Shen
Summary: This study found that X26nt is significantly elevated in gastric cancer and cancer cell exosomes, promoting the growth, migration, and tube formation of HUVECs. The research revealed how X26nt decreases VE-cadherin to increase vascular permeability and accelerates tumor growth and angiogenesis.