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Leukocyte extravasation and vascular permeability are each controlled in vivo by different tyrosine residues of VE-cadherin

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Leukocyte extravasation and vascular permeability are each controlled in vivo by different tyrosine residues of VE-cadherin. / Wessel, Florian; Winderlich, Mark; Holm, Maren; Frye, Maike; Rivera-Galdos, Ronmy; Vockel, Matthias; Linnepe, Ruth; Ipe, Ute; Stadtmann, Anika; Zarbock, Alexander; Nottebaum, Astrid F; Vestweber, Dietmar.

in: NAT IMMUNOL, Jahrgang 15, Nr. 3, 03.2014, S. 223-30.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Wessel, F, Winderlich, M, Holm, M, Frye, M, Rivera-Galdos, R, Vockel, M, Linnepe, R, Ipe, U, Stadtmann, A, Zarbock, A, Nottebaum, AF & Vestweber, D 2014, 'Leukocyte extravasation and vascular permeability are each controlled in vivo by different tyrosine residues of VE-cadherin', NAT IMMUNOL, Jg. 15, Nr. 3, S. 223-30. https://doi.org/10.1038/ni.2824

APA

Wessel, F., Winderlich, M., Holm, M., Frye, M., Rivera-Galdos, R., Vockel, M., Linnepe, R., Ipe, U., Stadtmann, A., Zarbock, A., Nottebaum, A. F., & Vestweber, D. (2014). Leukocyte extravasation and vascular permeability are each controlled in vivo by different tyrosine residues of VE-cadherin. NAT IMMUNOL, 15(3), 223-30. https://doi.org/10.1038/ni.2824

Vancouver

Wessel F, Winderlich M, Holm M, Frye M, Rivera-Galdos R, Vockel M et al. Leukocyte extravasation and vascular permeability are each controlled in vivo by different tyrosine residues of VE-cadherin. NAT IMMUNOL. 2014 Mär;15(3):223-30. https://doi.org/10.1038/ni.2824

Bibtex

@article{75d1c0578fd8444b8860b08a41f195b5,
title = "Leukocyte extravasation and vascular permeability are each controlled in vivo by different tyrosine residues of VE-cadherin",
abstract = "Tyrosine phosphorylation of the adhesion molecule VE-cadherin is assumed to affect endothelial junction integrity. However, it remains unclear whether tyrosine residues of VE-cadherin are required for the induction of vascular permeability and the regulation of leukocyte extravasation in vivo. We found here that knock-in mice expressing a Y685F mutant of VE-cadherin had impaired induction of vascular permeability, but those expressing a Y731F mutant did not. In contrast, mice expressing the Y731F VE-cadherin mutant showed decreased neutrophil-extravasation in cremaster tissue, but those expressing the Y685F mutant did not. Whereas inflammatory mediators induced the phosphorylation of Tyr685 in vivo, Tyr731 showed high baseline phosphorylation. Leukocytes triggered dephosphorylation of Tyr731 via the tyrosine phosphatase SHP-2, which allowed the adaptin AP-2 to bind and initiate endocytosis of VE-cadherin. Thus, Tyr685 and Tyr731 of VE-cadherin distinctly and selectively regulate the induction of vascular permeability or leukocyte extravasation. ",
keywords = "Animals, Antigens, CD/chemistry, Benzethonium/analogs & derivatives, Cadherins/chemistry, Capillary Permeability/physiology, Chemotaxis, Leukocyte/physiology, Endothelial Cells/metabolism, Fluorescent Antibody Technique, Gene Knock-In Techniques, Humans, Immunoblotting, Immunoprecipitation, Mice, Mice, Inbred C57BL, Phosphorylation, Tyrosine/metabolism",
author = "Florian Wessel and Mark Winderlich and Maren Holm and Maike Frye and Ronmy Rivera-Galdos and Matthias Vockel and Ruth Linnepe and Ute Ipe and Anika Stadtmann and Alexander Zarbock and Nottebaum, {Astrid F} and Dietmar Vestweber",
year = "2014",
month = mar,
doi = "10.1038/ni.2824",
language = "English",
volume = "15",
pages = "223--30",
journal = "NAT IMMUNOL",
issn = "1529-2908",
publisher = "NATURE PUBLISHING GROUP",
number = "3",

}

RIS

TY - JOUR

T1 - Leukocyte extravasation and vascular permeability are each controlled in vivo by different tyrosine residues of VE-cadherin

AU - Wessel, Florian

AU - Winderlich, Mark

AU - Holm, Maren

AU - Frye, Maike

AU - Rivera-Galdos, Ronmy

AU - Vockel, Matthias

AU - Linnepe, Ruth

AU - Ipe, Ute

AU - Stadtmann, Anika

AU - Zarbock, Alexander

AU - Nottebaum, Astrid F

AU - Vestweber, Dietmar

PY - 2014/3

Y1 - 2014/3

N2 - Tyrosine phosphorylation of the adhesion molecule VE-cadherin is assumed to affect endothelial junction integrity. However, it remains unclear whether tyrosine residues of VE-cadherin are required for the induction of vascular permeability and the regulation of leukocyte extravasation in vivo. We found here that knock-in mice expressing a Y685F mutant of VE-cadherin had impaired induction of vascular permeability, but those expressing a Y731F mutant did not. In contrast, mice expressing the Y731F VE-cadherin mutant showed decreased neutrophil-extravasation in cremaster tissue, but those expressing the Y685F mutant did not. Whereas inflammatory mediators induced the phosphorylation of Tyr685 in vivo, Tyr731 showed high baseline phosphorylation. Leukocytes triggered dephosphorylation of Tyr731 via the tyrosine phosphatase SHP-2, which allowed the adaptin AP-2 to bind and initiate endocytosis of VE-cadherin. Thus, Tyr685 and Tyr731 of VE-cadherin distinctly and selectively regulate the induction of vascular permeability or leukocyte extravasation.

AB - Tyrosine phosphorylation of the adhesion molecule VE-cadherin is assumed to affect endothelial junction integrity. However, it remains unclear whether tyrosine residues of VE-cadherin are required for the induction of vascular permeability and the regulation of leukocyte extravasation in vivo. We found here that knock-in mice expressing a Y685F mutant of VE-cadherin had impaired induction of vascular permeability, but those expressing a Y731F mutant did not. In contrast, mice expressing the Y731F VE-cadherin mutant showed decreased neutrophil-extravasation in cremaster tissue, but those expressing the Y685F mutant did not. Whereas inflammatory mediators induced the phosphorylation of Tyr685 in vivo, Tyr731 showed high baseline phosphorylation. Leukocytes triggered dephosphorylation of Tyr731 via the tyrosine phosphatase SHP-2, which allowed the adaptin AP-2 to bind and initiate endocytosis of VE-cadherin. Thus, Tyr685 and Tyr731 of VE-cadherin distinctly and selectively regulate the induction of vascular permeability or leukocyte extravasation.

KW - Animals

KW - Antigens, CD/chemistry

KW - Benzethonium/analogs & derivatives

KW - Cadherins/chemistry

KW - Capillary Permeability/physiology

KW - Chemotaxis, Leukocyte/physiology

KW - Endothelial Cells/metabolism

KW - Fluorescent Antibody Technique

KW - Gene Knock-In Techniques

KW - Humans

KW - Immunoblotting

KW - Immunoprecipitation

KW - Mice

KW - Mice, Inbred C57BL

KW - Phosphorylation

KW - Tyrosine/metabolism

U2 - 10.1038/ni.2824

DO - 10.1038/ni.2824

M3 - SCORING: Journal article

C2 - 24487320

VL - 15

SP - 223

EP - 230

JO - NAT IMMUNOL

JF - NAT IMMUNOL

SN - 1529-2908

IS - 3

ER -