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1,219 results on '"Dejana, Elisabetta"'

1. GPR126 is a specifier of blood-brain barrier formation in the mouse central nervous system

Author

Kakogiannos, Nikolaos, Scalise, Anna Agata, Martini, Emanuele, Maderna, Claudio, Benvenuto, Andrea Francesco, D'Antonio, Michele, Carmignani, Laura, Magni, Serena, Gullotta, Giorgia Serena, Lampugnani, Maria Grazia, Iannelli, Fabio, Beznoussenko, Galina V., Mironov, Alexander A., Cerutti, Camilla, Bentley, Katie, Philippides, Andrew, Zanardi, Federica, Bacigaluppi, Marco, Sigismund, Sara, Bassani, Claudia, Farina, Cinthia, Martino, Gianvito, De Giovanni, Marco, Dejana, Elisabetta, Iannacone, Matteo, Inverso, Donato, and Giannotta, Monica

Subjects
G proteins -- Physiological aspects, Blood-brain barrier -- Physiological aspects, Cell receptors -- Analysis, Central nervous system -- Models -- Physiological aspects, Health care industry
Abstract

The blood-brain barrier (BBB) acquires unique properties to regulate neuronal function during development. The formation of the BBB, which occurs in tandem with angiogenesis, is directed by the Wnt/[beta]-catenin signaling pathway. Yet the exact molecular interplay remains elusive. Our study reveals the G protein-coupled receptor GPR126 as a critical target of canonical Wnt signaling, essential for the development of the BBB's distinctive vascular characteristics and its functional integrity. Endothelial cell-specific deletion of the Gpr126 gene in mice induced aberrant vascular morphogenesis, resulting in disrupted BBB organization. Simultaneously, heightened transcytosis in vitro compromised barrier integrity, resulting in enhanced vascular permeability. Mechanistically, GPR126 enhanced endothelial cell migration, pivotal for angiogenesis, acting through an interaction between LRP1 and [[beta].sub.1] integrin, thereby balancing the levels of [[beta].sub.1] integrin activation and recycling. Overall, we identified GPR126 as a specifier of an organotypic vascular structure, which sustained angiogenesis and guaranteed the acquisition of the BBB properties during development., Introduction The blood-brain barrier (BBB) separates the neural tissue from the blood circulation. The BBB is formed by a single layer of the endothelial cells (ECs) that line the blood [...]

Published
2024
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2. Magnetic susceptibility as a 1-year predictor of outcome in familial cerebral cavernous malformations: a pilot study

Author

Incerti, Irene, Fusco, Massimo, Contarino, Valeria Elisa, Siggillino, Silvia, Conte, Giorgio, Lanfranconi, Silvia, Bertani, Giulio Andrea, Gaudino, Chiara, d’Orio, Piergiorgio, Pallini, Roberto, D’Alessandris, Quintino Giorgio, Meessen, Jennifer Marie Theresia Anna, Nicolis, Enrico Bjorn, Vasamì, Antonella, Dejana, Elisabetta, Bianchi, Anna Maria, Triulzi, Fabio Maria, Latini, Roberto, and Scola, Elisa

Published
2023
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3. Circulating biomarkers in familial cerebral cavernous malformation

Author

Lazzaroni, Francesca, Meessen, Jennifer M.T.A., Sun, Ying, Lanfranconi, Silvia, Scola, Elisa, D'Alessandris, Quintino Giorgio, Tassi, Laura, Carriero, Maria Rita, Castori, Marco, Marino, Silvia, Blanda, Adriana, Nicolis, Enrico B., Novelli, Deborah, Calabrese, Roberta, Agnelli, Nicolò M., Bottazzi, Barbara, Leone, Roberto, Mazzola, Selene, Besana, Silvia, Catozzi, Carlotta, Nezi, Luigi, Lampugnani, Maria G., Malinverno, Matteo, Grdseloff, Nastasja, Rödel, Claudia J., Rezai Jahromi, Behnam, Bolli, Niccolò, Passamonti, Francesco, Magnusson, Peetra U., Abdelilah-Seyfried, Salim, Dejana, Elisabetta, and Latini, Roberto

Published
2024
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4. Permeability of the Endothelial Barrier: Identifying and Reconciling Controversies

Author

Claesson-Welsh, Lena, Dejana, Elisabetta, and McDonald, Donald M

Subjects
Aetiology, 2.1 Biological and endogenous factors, Cardiovascular, Good Health and Well Being, Animals, Capillary Permeability, Endothelial Cells, Endothelial Growth Factors, Endothelium, Vascular, Humans, Intercellular Junctions, Receptors, Opioid, Receptors, Vascular Endothelial Growth Factor, Signal Transduction, Vascular Endothelial Growth Factor A, rho GTP-Binding Proteins, G protein-coupled receptors, Rho GTPases, VEGF receptors, endothelial barrier function, endothelial cell junctions, gap formation, postcapillary venules, Biological Sciences, Medical and Health Sciences, Immunology
Abstract

Leakage from blood vessels into tissues is governed by mechanisms that control endothelial barrier function to maintain homeostasis. Dysregulated endothelial permeability contributes to many conditions and can influence disease morbidity and treatment. Diverse approaches used to study endothelial permeability have yielded a wealth of valuable insights. Yet, ongoing questions, technical challenges, and unresolved controversies relating to the mechanisms and relative contributions of barrier regulation, transendothelial sieving, and transport of fluid, solutes, and particulates complicate interpretations in the context of vascular physiology and pathophysiology. Here, we describe recent in vivo findings and other advances in understanding endothelial barrier function with the goal of identifying and reconciling controversies over cellular and molecular processes that regulate the vascular barrier in health and disease.

Published
2021

5. Safety and efficacy of propranolol for treatment of familial cerebral cavernous malformations (Treat_CCM): a randomised, open-label, blinded-endpoint, phase 2 pilot trial

Author

Abete Fornara, Giorgia, Agnelli, Nicolò M., Albanese, Alessio, Awad, Issam, Bagnati, Renzo, Balconi, Giovanna, Ballabio, Elena, Beghi, Ettore, Bernasconi, Roberto, Bertani, Giulio A., Besana, Silvia, Blanda, Adriana, Bossi, Chiara, Bresolin, Nereo, Buratti, Maria G., Calabrese, Roberta, Carriero, Maria R., Castori, Marco, Ciceri, Elisa F., Ciurleo, Rossella, Comi, Giacomo P., Contarino, Valeria, Conte, Giorgio, D'Agruma, Leonardo, D'Alessandris, Giorgio Q., de Grazia, Ugo, Di Bonaventura, Rina, d'Orio, Piergiorgio, Farago', Giuseppe, Foresta, Andreana, Fusco, Carmela, Gaudino, Chiara, Lampugnani, Maria G., Lanno, Alessia, Lazzaroni, Francesca, Lee, Cornelia, Locatelli, Marco, Maggioni, Aldo P., Magnusson, Peetra, Malinverno, Matteo, Mangiavacchi, Maurizio, Mangraviti, Antonella, Marino, Silvia, Mazzola, Selene, Nicolis, Enrico B., Novelli, Deborah, Ojeda Fernandez, Maria L., Petracca, Antonio, Pignotti, Fabrizio, Pogliani, Simona, Poloni, Marco, Prelle, Alessandro, Raggi, Pamela, Raucci, Franca, Regna-Gladin, Caroline, Ronchi, Dario, Scelzo, Emma, Seyfried, Salim, Simeone, Anna, Sturiale, Carmelo L., Tassi, Laura, Tettamanti, Mauro, Torri, Valter, Tournier-Lasserve, Elisabeth, Treglia, Rita, Triulzi, Fabio M., Ungaro, Celeste, Ursi, Elison, Valcamonica, Gloria, Vasami', Antonella, Zarino, Barbara, Lanfranconi, Silvia, Scola, Elisa, Meessen, Jennifer M T A, Pallini, Roberto, Bertani, Giulio A, Al-Shahi Salman, Rustam, Dejana, Elisabetta, and Latini, Roberto

Published
2023
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6. Immunothrombosis and vascular heterogeneity in cerebral cavernous malformation

Author

Globisch, Maria A., Onyeogaziri, Favour C., Jauhiainen, Suvi, Yau, Anthony C.Y., Orsenigo, Fabrizio, Conze, Lei L., Arce, Maximiliano, Corada, Monica, Smith, Ross O., Rorsman, Charlotte, Sundell, Veronica, Fernando, Dinesh, Daniel, Geoffrey, Mattsson, Oscar, Savander, Henri, Wanders, Alkwin, Rezai Jahromi, Behnam, Laakso, Aki, Niemelä, Mika, Dejana, Elisabetta, and Magnusson, Peetra U.

Published
2022
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7. Correction: Inflammation and neutrophil extracellular traps in cerebral cavernous malformation

Author

Yau, Anthony C. Y., Globisch, Maria Ascencion, Onyeogaziri, Favour Chinyere, Conze, Lei L., Smith, Ross, Jauhiainen, Suvi, Corada, Monica, Orsenigo, Fabrizio, Huang, Hua, Herre, Melanie, Olsson, Anna-Karin, Malinverno, Matteo, Sundell, Veronica, Rezai Jahromi, Behnam, Niemelä, Mika, Laakso, Aki, Garlanda, Cecilia, Mantovani, Alberto, Lampugnani, Maria Grazia, Dejana, Elisabetta, and Magnusson, Peetra U.

Published
2022
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10. Inflammation and neutrophil extracellular traps in cerebral cavernous malformation

Author

Yau, Anthony C. Y., Globisch, Maria Ascencion, Onyeogaziri, Favour Chinyere, Conze, Lei L., Smith, Ross, Jauhiainen, Suvi, Corada, Monica, Orsenigo, Fabrizio, Huang, Hua, Herre, Melanie, Olsson, Anna-Karin, Malinverno, Matteo, Sundell, Veronica, Rezai Jahromi, Behnam, Niemelä, Mika, Laakso, Aki, Garlanda, Cecilia, Mantovani, Alberto, Lampugnani, Maria Grazia, Dejana, Elisabetta, and Magnusson, Peetra U.

Published
2022
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12. Inhibition of endothelial FAK activity prevents tumor metastasis by enhancing barrier function

Author

Jean, Christine, Chen, Xiao Lei, Nam, Ju-Ock, Tancioni, Isabelle, Uryu, Sean, Lawson, Christine, Ward, Kristy K, Walsh, Colin T, Miller, Nichol LG, Ghassemian, Majid, Turowski, Patric, Dejana, Elisabetta, Weis, Sara, Cheresh, David A, and Schlaepfer, David D

Subjects
Biochemistry and Cell Biology, Medical Physiology, Biomedical and Clinical Sciences, Biological Sciences, Cancer, Rare Diseases, 2.1 Biological and endogenous factors, Aetiology, Cardiovascular, Animals, Antigens, CD, Cadherins, Cell Movement, Focal Adhesion Protein-Tyrosine Kinases, HEK293 Cells, Humans, Mice, Mice, Inbred BALB C, Neoplasm Metastasis, Phosphorylation, Proto-Oncogene Proteins pp60(c-src), Signal Transduction, Vascular Endothelial Growth Factor A, Vascular Endothelial Growth Factor Receptor-2, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

Pharmacological focal adhesion kinase (FAK) inhibition prevents tumor growth and metastasis, via actions on both tumor and stromal cells. In this paper, we show that vascular endothelial cadherin (VEC) tyrosine (Y) 658 is a target of FAK in tumor-associated endothelial cells (ECs). Conditional kinase-dead FAK knockin within ECs inhibited recombinant vascular endothelial growth factor (VEGF-A) and tumor-induced VEC-Y658 phosphorylation in vivo. Adherence of VEGF-expressing tumor cells to ECs triggered FAK-dependent VEC-Y658 phosphorylation. Both FAK inhibition and VEC-Y658F mutation within ECs prevented VEGF-initiated paracellular permeability and tumor cell transmigration across EC barriers. In mice, EC FAK inhibition prevented VEGF-dependent tumor cell extravasation and melanoma dermal to lung metastasis without affecting primary tumor growth. As pharmacological c-Src or FAK inhibition prevents VEGF-stimulated c-Src and FAK translocation to EC adherens junctions, but FAK inhibition does not alter c-Src activation, our experiments identify EC FAK as a key intermediate between c-Src and the regulation of EC barrier function controlling tumor metastasis.

Published
2014

13. Progesterone Receptor in the Vascular Endothelium Triggers Physiological Uterine Permeability Preimplantation

Author

Goddard, Lauren M, Murphy, Thomas J, Org, Tönis, Enciso, Josephine M, Hashimoto-Partyka, Minako K, Warren, Carmen M, Domigan, Courtney K, McDonald, Austin I, He, Huanhuan, Sanchez, Lauren A, Allen, Nancy C, Orsenigo, Fabrizio, Chao, Lily C, Dejana, Elisabetta, Tontonoz, Peter, Mikkola, Hanna KA, and Iruela-Arispe, M Luisa

Subjects
Clinical Research, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Aetiology, Underpinning research, Cardiovascular, Animals, Capillary Permeability, Endometrium, Endothelium, Vascular, Female, Gene Expression Regulation, Humans, Mice, Nuclear Receptor Subfamily 4, Group A, Member 1, Uterus, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Vascular permeability is frequently associated with inflammation and is triggered by a cohort of secreted permeability factors such as vascular endothelial growth factor (VEGF). Here, we show that the physiological vascular permeability that precedes implantation is directly controlled by progesterone receptor (PR) and is independent of VEGF. Global or endothelial-specific deletion of PR blocks physiological vascular permeability in the uterus, whereas misexpression of PR in the endothelium of other organs results in ectopic vascular leakage. Integration of an endothelial genome-wide transcriptional profile with chromatin immunoprecipitation sequencing revealed that PR induces an NR4A1 (Nur77/TR3)-dependent transcriptional program that broadly regulates vascular permeability in response to progesterone. Silencing of NR4A1 blocks PR-mediated permeability responses, indicating a direct link between PR and NR4A1. This program triggers concurrent suppression of several junctional proteins and leads to an effective, timely, and venous-specific regulation of vascular barrier function that is critical for embryo implantation.

Published
2014

16. Sox17 is indispensable for acquisition and maintenance of arterial identity

Author

Corada, Monica, Orsenigo, Fabrizio, Morini, Marco Francesco, Pitulescu, Mara Elena, Bhat, Ganesh, Nyqvist, Daniel, Breviario, Ferruccio, Conti, Valentina, Briot, Anais, Iruela-Arispe, M Luisa, Adams, Ralf H, and Dejana, Elisabetta

Subjects
Pediatric, 1.1 Normal biological development and functioning, Underpinning research, Cardiovascular, Animals, Arteries, Cell Differentiation, Cell Proliferation, Embryo, Mammalian, Endoderm, Endothelial Cells, Gene Expression Regulation, Developmental, HMGB Proteins, Mice, Morphogenesis, Neovascularization, Pathologic, Receptors, Notch, Retina, SOXF Transcription Factors, Signal Transduction, Veins, Wnt Proteins
Abstract

The functional diversity of the arterial and venous endothelia is regulated through a complex system of signalling pathways and downstream transcription factors. Here we report that the transcription factor Sox17, which is known as a regulator of endoderm and hemopoietic differentiation, is selectively expressed in arteries, and not in veins, in the mouse embryo and in mouse postnatal retina and adult. Endothelial cell-specific inactivation of Sox17 in the mouse embryo is accompanied by a lack of arterial differentiation and vascular remodelling that results in embryo death in utero. In mouse postnatal retina, abrogation of Sox17 expression in endothelial cells leads to strong vascular hypersprouting, loss of arterial identity and large arteriovenous malformations. Mechanistically, Sox17 acts upstream of the Notch system and downstream of the canonical Wnt system. These data introduce Sox17 as a component of the complex signalling network that orchestrates arterial/venous specification.

Published
2013

17. Propranolol Reduces the Development of Lesions and Rescues Barrier Function in Cerebral Cavernous Malformations: A Preclinical Study

Author

Oldenburg, Joppe, Malinverno, Matteo, Globisch, Maria Ascencion, Maderna, Claudio, Corada, Monica, Orsenigo, Fabrizio, Conze, Lei Liu, Rorsman, Charlotte, Sundell, Veronica, Arce, Maximiliano, Smith, Ross O., Yau, Anthony C.Y., Billström, Gry Hulsart, Mägi, Caroline Öhman, Beznoussenko, Galina V., Mironov, Alexander A., Fernando, Dinesh, Daniel, Geoffrey, Olivari, Davide, Fumagalli, Francesca, Lampugnani, Maria Grazia, Dejana, Elisabetta, and Magnusson, Peetra U.

Published
2021
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18. Phosphorylation of VE-cadherin is modulated by haemodynamic forces and contributes to the regulation of vascular permeability in vivo.

Author

Orsenigo, Fabrizio, Giampietro, Costanza, Ferrari, Aldo, Corada, Monica, Galaup, Ariane, Sigismund, Sara, Ristagno, Giuseppe, Maddaluno, Luigi, Koh, Gou Young, Franco, Davide, Kurtcuoglu, Vartan, Poulikakos, Dimos, Baluk, Peter, McDonald, Donald, Grazia Lampugnani, Maria, and Dejana, Elisabetta

Subjects
Arteries, Veins, Animals, Mice, Inbred C57BL, Humans, Mice, src-Family Kinases, Bradykinin, Cadherins, Inflammation Mediators, Antigens, CD, Endocytosis, Antibody Specificity, Enzyme Activation, Amino Acid Sequence, Capillary Permeability, Phosphorylation, Stress, Mechanical, Molecular Sequence Data, Hemodynamics, Ubiquitination, Human Umbilical Vein Endothelial Cells, Inbred C57BL, Antigens, CD, Stress, Mechanical
Abstract

Endothelial adherens junctions maintain vascular integrity. Arteries and veins differ in their permeability but whether organization and strength of their adherens junctions vary has not been demonstrated in vivo. Here we report that vascular endothelial cadherin, an endothelial specific adhesion protein located at adherens junctions, is phosphorylated in Y658 and Y685 in vivo in veins but not in arteries under resting conditions. This difference is due to shear stress-induced junctional Src activation in veins. Phosphorylated vascular endothelial-cadherin is internalized and ubiquitinated in response to permeability-increasing agents such as bradykinin and histamine. Inhibition of Src blocks vascular endothelial cadherin phosphorylation and bradykinin-induced permeability. Point mutation of Y658F and Y685F prevents vascular endothelial cadherin internalization, ubiquitination and an increase in permeability by bradykinin in vitro. Thus, phosphorylation of vascular endothelial cadherin contributes to a dynamic state of adherens junctions, but is not sufficient to increase vascular permeability in the absence of inflammatory agents.

Published
2012

25. Functionally specialized junctions between endothelial cells of lymphatic vessels

Author

Baluk, Peter, Fuxe, Jonas, Hashizume, Hiroya, Romano, Talia, Lashnits, Erin, Butz, Stefan, Vestweber, Dietmar, Corada, Monica, Molendini, Cinzia, Dejana, Elisabetta, and McDonald, Donald M

Subjects
1.1 Normal biological development and functioning, Underpinning research, Animals, Cadherins, Cell Movement, Endothelial Cells, Lymphatic Vessels, Lymphocytes, Mice, Mice, Inbred C57BL, Platelet Endothelial Cell Adhesion Molecule-1, Medical and Health Sciences, Immunology
Abstract

Recirculation of fluid and cells through lymphatic vessels plays a key role in normal tissue homeostasis, inflammatory diseases, and cancer. Despite recent advances in understanding lymphatic function (Alitalo, K., T. Tammela, and T.V. Petrova. 2005. Nature. 438:946-953), the cellular features responsible for entry of fluid and cells into lymphatics are incompletely understood. We report the presence of novel junctions between endothelial cells of initial lymphatics at likely sites of fluid entry. Overlapping flaps at borders of oak leaf-shaped endothelial cells of initial lymphatics lacked junctions at the tip but were anchored on the sides by discontinuous button-like junctions (buttons) that differed from conventional, continuous, zipper-like junctions (zippers) in collecting lymphatics and blood vessels. However, both buttons and zippers were composed of vascular endothelial cadherin (VE-cadherin) and tight junction-associated proteins, including occludin, claudin-5, zonula occludens-1, junctional adhesion molecule-A, and endothelial cell-selective adhesion molecule. In C57BL/6 mice, VE-cadherin was required for maintenance of junctional integrity, but platelet/endothelial cell adhesion molecule-1 was not. Growing tips of lymphatic sprouts had zippers, not buttons, suggesting that buttons are specialized junctions rather than immature ones. Our findings suggest that fluid enters throughout initial lymphatics via openings between buttons, which open and close without disrupting junctional integrity, but most leukocytes enter the proximal half of initial lymphatics.

Published
2007

26. JAM-A Acts via C/EBP-α to Promote Claudin-5 Expression and Enhance Endothelial Barrier Function

Author

Kakogiannos, Nikolaos, Ferrari, Laura, Giampietro, Costanza, Scalise, Anna Agata, Maderna, Claudio, Ravà, Micol, Taddei, Andrea, Lampugnani, Maria Grazia, Pisati, Federica, Malinverno, Matteo, Martini, Emanuele, Costa, Ilaria, Lupia, Michela, Cavallaro, Ugo, Beznoussenko, Galina V., Mironov, Alexander A., Fernandes, Bethania, Rudini, Noemi, Dejana, Elisabetta, and Giannotta, Monica

Published
2020
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28. CD93 promotes [[beta].sub.1] integrin activation and fibronectin fibrillogenesis during tumor angiogenesis

Author

Lugano, Roberta, Vemuri, Kalyani, Yu, Di, Bergqvist, Michael, Smits, Anja, Essand, Magnus, Johansson, Staffan, Dejana, Elisabetta, and Dimberg, Anna

Subjects
Extracellular matrix -- Research, Neovascularization -- Research, Fibronectins -- Analysis, Gene expression -- Research, Glioblastomas -- Research -- Genetic aspects, Health care industry
Abstract

Tumor angiogenesis occurs through regulation of genes that orchestrate endothelial sprouting and vessel maturation, including deposition of a vessel-associated extracellular matrix. CD93 is a transmembrane receptor that is upregulated in tumor vessels in many cancers, including high-grade glioma. Here, we demonstrate that CD93 regulates [[beta].sub.1] integrin signaling and organization of fibronectin fibrillogenesis during tumor vascularization. In endothelial cells and mouse retina, CD93 was found to be expressed in endothelial filopodia and to promote filopodia formation. The CD93 localization to endothelial filopodia was stabilized by interaction with multimerin-2 (MMRN2), which inhibited its proteolytic cleavage. The CD93- MMRN2 complex was required for activation of [[beta].sub.1] integrin, phosphorylation of focal adhesion kinase (FAK), and fibronectin fibrillogenesis in endothelial cells. Consequently, tumor vessels in gliomas implanted orthotopically in CD93-deficient mice showed diminished activation of [[beta].sub.1] integrin and lacked organization of fibronectin into fibrillar structures. These findings demonstrate a key role of CD93 in vascular maturation and organization of the extracellular matrix in tumors, identifying it as a potential target for therapy., Introduction Gliomas are common brain tumors that occur as ependymomas, oligodendrogliomas, and astrocytomas of WHO grades I-IV (1). Glioblastoma (WHO grade IV), the most malignant and common form of glioma, [...]

Published
2018
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33. FigS1,FigS2,FigS3,FigS4,FigS5,FigS6 from Targeting Vascular Endothelial-Cadherin in Tumor-Associated Blood Vessels Promotes T-cell–Mediated Immunotherapy

Author

Zhao, Yang, primary, Ting, Ka Ka, primary, Li, Jia, primary, Cogger, Victoria C., primary, Chen, Jinbiao, primary, Johansson-Percival, Anna, primary, Ngiow, Shin Foong, primary, Holst, Jeff, primary, Grau, Georges, primary, Goel, Shom, primary, Muller, Thorleif, primary, Dejana, Elisabetta, primary, McCaughan, Geoff, primary, Smyth, Mark J., primary, Ganss, Ruth, primary, Vadas, Mathew A., primary, and Gamble, Jennifer R., primary

Published
2023
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34. Supplemental figures 1-6 from Targeting Vascular Endothelial-Cadherin in Tumor-Associated Blood Vessels Promotes T-cell–Mediated Immunotherapy

Author

Zhao, Yang, primary, Ting, Ka Ka, primary, Li, Jia, primary, Cogger, Victoria C., primary, Chen, Jinbiao, primary, Johansson-Percival, Anna, primary, Ngiow, Shin Foong, primary, Holst, Jeff, primary, Grau, Georges, primary, Goel, Shom, primary, Muller, Thorleif, primary, Dejana, Elisabetta, primary, McCaughan, Geoff, primary, Smyth, Mark J., primary, Ganss, Ruth, primary, Vadas, Mathew A., primary, and Gamble, Jennifer R., primary

Published
2023
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35. Data from Targeting Vascular Endothelial-Cadherin in Tumor-Associated Blood Vessels Promotes T-cell–Mediated Immunotherapy

Author

Zhao, Yang, primary, Ting, Ka Ka, primary, Li, Jia, primary, Cogger, Victoria C., primary, Chen, Jinbiao, primary, Johansson-Percival, Anna, primary, Ngiow, Shin Foong, primary, Holst, Jeff, primary, Grau, Georges, primary, Goel, Shom, primary, Muller, Thorleif, primary, Dejana, Elisabetta, primary, McCaughan, Geoff, primary, Smyth, Mark J., primary, Ganss, Ruth, primary, Vadas, Mathew A., primary, and Gamble, Jennifer R., primary

Published
2023
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36. Table and material & methods from Targeting Vascular Endothelial-Cadherin in Tumor-Associated Blood Vessels Promotes T-cell–Mediated Immunotherapy

Author

Zhao, Yang, primary, Ting, Ka Ka, primary, Li, Jia, primary, Cogger, Victoria C., primary, Chen, Jinbiao, primary, Johansson-Percival, Anna, primary, Ngiow, Shin Foong, primary, Holst, Jeff, primary, Grau, Georges, primary, Goel, Shom, primary, Muller, Thorleif, primary, Dejana, Elisabetta, primary, McCaughan, Geoff, primary, Smyth, Mark J., primary, Ganss, Ruth, primary, Vadas, Mathew A., primary, and Gamble, Jennifer R., primary

Published
2023
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37. Supplementary Figure 4 from Inactivation of Junctional Adhesion Molecule-A Enhances Antitumoral Immune Response by Promoting Dendritic Cell and T Lymphocyte Infiltration

Author

Murakami, Masato, primary, Francavilla, Chiara, primary, Torselli, Ilaria, primary, Corada, Monica, primary, Maddaluno, Luigi, primary, Sica, Antonio, primary, Matteoli, Gianluca, primary, Iliev, Iliyan Dimitrov, primary, Mantovani, Alberto, primary, Rescigno, Maria, primary, Cavallaro, Ugo, primary, and Dejana, Elisabetta, primary

Published
2023
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38. Supplementary Figure 5 from Inactivation of Junctional Adhesion Molecule-A Enhances Antitumoral Immune Response by Promoting Dendritic Cell and T Lymphocyte Infiltration

Author

Murakami, Masato, primary, Francavilla, Chiara, primary, Torselli, Ilaria, primary, Corada, Monica, primary, Maddaluno, Luigi, primary, Sica, Antonio, primary, Matteoli, Gianluca, primary, Iliev, Iliyan Dimitrov, primary, Mantovani, Alberto, primary, Rescigno, Maria, primary, Cavallaro, Ugo, primary, and Dejana, Elisabetta, primary

Published
2023
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39. Data from Inactivation of Junctional Adhesion Molecule-A Enhances Antitumoral Immune Response by Promoting Dendritic Cell and T Lymphocyte Infiltration

Author

Murakami, Masato, primary, Francavilla, Chiara, primary, Torselli, Ilaria, primary, Corada, Monica, primary, Maddaluno, Luigi, primary, Sica, Antonio, primary, Matteoli, Gianluca, primary, Iliev, Iliyan Dimitrov, primary, Mantovani, Alberto, primary, Rescigno, Maria, primary, Cavallaro, Ugo, primary, and Dejana, Elisabetta, primary

Published
2023
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40. Supplementary Figure 1 from Inactivation of Junctional Adhesion Molecule-A Enhances Antitumoral Immune Response by Promoting Dendritic Cell and T Lymphocyte Infiltration

Author

Murakami, Masato, primary, Francavilla, Chiara, primary, Torselli, Ilaria, primary, Corada, Monica, primary, Maddaluno, Luigi, primary, Sica, Antonio, primary, Matteoli, Gianluca, primary, Iliev, Iliyan Dimitrov, primary, Mantovani, Alberto, primary, Rescigno, Maria, primary, Cavallaro, Ugo, primary, and Dejana, Elisabetta, primary

Published
2023
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41. Supplementary Methods, Figure Legends 1-5 from Inactivation of Junctional Adhesion Molecule-A Enhances Antitumoral Immune Response by Promoting Dendritic Cell and T Lymphocyte Infiltration

Author

Murakami, Masato, primary, Francavilla, Chiara, primary, Torselli, Ilaria, primary, Corada, Monica, primary, Maddaluno, Luigi, primary, Sica, Antonio, primary, Matteoli, Gianluca, primary, Iliev, Iliyan Dimitrov, primary, Mantovani, Alberto, primary, Rescigno, Maria, primary, Cavallaro, Ugo, primary, and Dejana, Elisabetta, primary

Published
2023
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42. Supplementary Figure 2 from Inactivation of Junctional Adhesion Molecule-A Enhances Antitumoral Immune Response by Promoting Dendritic Cell and T Lymphocyte Infiltration

Author

Murakami, Masato, primary, Francavilla, Chiara, primary, Torselli, Ilaria, primary, Corada, Monica, primary, Maddaluno, Luigi, primary, Sica, Antonio, primary, Matteoli, Gianluca, primary, Iliev, Iliyan Dimitrov, primary, Mantovani, Alberto, primary, Rescigno, Maria, primary, Cavallaro, Ugo, primary, and Dejana, Elisabetta, primary

Published
2023
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43. Supplementary Figure 3 from Inactivation of Junctional Adhesion Molecule-A Enhances Antitumoral Immune Response by Promoting Dendritic Cell and T Lymphocyte Infiltration

Author

Murakami, Masato, primary, Francavilla, Chiara, primary, Torselli, Ilaria, primary, Corada, Monica, primary, Maddaluno, Luigi, primary, Sica, Antonio, primary, Matteoli, Gianluca, primary, Iliev, Iliyan Dimitrov, primary, Mantovani, Alberto, primary, Rescigno, Maria, primary, Cavallaro, Ugo, primary, and Dejana, Elisabetta, primary

Published
2023
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46. CD93 maintains endothelial barrier function by limiting the phosphorylation and turnover of VE-cadherin

Author

Lugano, Roberta, Vemuri, Kalyani, Barbera, Stefano, Orlandini, Maurizio, Dejana, Elisabetta, Claesson-Welsh, Lena, Dimberg, Anna, Lugano, Roberta, Vemuri, Kalyani, Barbera, Stefano, Orlandini, Maurizio, Dejana, Elisabetta, Claesson-Welsh, Lena, and Dimberg, Anna

Abstract

Regulation of vascular permeability to plasma is essential for tissue and organ homeostasis and is mediated by endothelial cell-to-cell junctions that tightly regulate the trafficking of molecules between blood and tissue. The single-pass transmembrane glycoprotein CD93 is upregulated in endothelial cells during angiogenesis and controls cytoskeletal dynamics. However, its role in maintaining homeostasis by regulating endothelial barrier function has not been elucidated yet. Here, we demonstrate that CD93 interacts with vascular endothelial (VE)-cadherin and limits its phosphorylation and turnover. CD93 deficiency in vitro and in vivo induces phosphorylation of VE-cadherin under basal conditions, displacing it from endothelial cell–cell contacts. Consistent with this, endothelial junctions are defective in CD93−/− mice, and the blood–brain barrier permeability is enhanced. Mechanistically, CD93 regulates VE-cadherin phosphorylation and turnover at endothelial junctions through the Rho/Rho kinase-dependent pathway. In conclusion, our results identify CD93 as a key regulator of VE-cadherin stability at endothelial junctions, opening up possibilities for therapeutic strategies directed to control vascular permeability.

Published
2023
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