NDLI: Src Phosphorylation of Endothelial Cell Surface Intercellular Adhesion Molecule-1 Mediates Neutrophil Adhesion and Contributes to the Mechanism of Lung Inflammation

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Src Phosphorylation of Endothelial Cell Surface Intercellular Adhesion Molecule-1 Mediates Neutrophil Adhesion and Contributes to the Mechanism of Lung Inflammation

Content Provider	Scilit
Author	Liu, Guoquan Vogel, Stephen M. Gao, Xiao Pei Javaid, Kamran Hu, Guochang Danilov, Sergei M. Malik, Asrar B. Minshall, Richard D.
Copyright Year	2011
Description	Journal: Arteriosclerosis, thrombosis, and vascular biology The goal of this study was to determine whether tumor necrosis factor α (TNFα)–induced Src activation and intercellular adhesion molecule-1 (ICAM-1) phosphorylation rapidly increase endothelial cell adhesivity and polymorphonuclear leukocyte (PMN) sequestration independently of de novo ICAM-1 synthesis. TNFα exposure of mouse lungs for 5 minutes produced a 3-fold increase in$ ^{125}$ I-anti-ICAM-1 monoclonal antibody (mAb) binding and$ ^{111}$ In oxine-labeled PMN sequestration, as well as Src activation, ICAM-1 Tyr518 phosphorylation, and phospho- Tyr518-ICAM-1 coimmunoprecipitation with actin. The response was absent in Nox2$ ^{−/−}$ lungs or following Src inhibition. In COS-7 cells transfected with wild-type (WT), phospho-defective (Tyr518Phe), or phospho-mimicking (Tyr518Asp) mouse ICAM-1 cDNA constructs, TNFα increased the B$ _{max}$ of YN1/1.7.4 anti-ICAM-1 mAb binding to WT-ICAM-1 but not to Tyr518Phe-ICAM-1, indicating increased binding avidity secondary to ICAM-1 phosphorylation. This effect was mimicked by expression of the Tyr518Asp-ICAM-1 mutant. TNFα also increased the staining intensity and cell surface clustering of YN1/1.7.4 mAb-labeled WT-ICAM-1 that colocalized with F-actin, which was not observed with Tyr518Phe-ICAM-1 but was recapitulated with Tyr518Asp-ICAM-1. Finally, overexpression of ICAM-1 in mouse lungs significantly increased lipopolysaccharide-induced transvascular albumin leakage and bronchoalveolar lavage PMN counts at 2 and 24 hours after lipopolysaccharide inhalation compared with lungs expressing the Tyr518Phe ICAM-1 mutant. Src-dependent phosphorylation of endothelial cell ICAM-1 Tyr518 induces PMN adhesion by promoting ICAM-1 clustering, which we propose mediates rapid-phase lung vascular accumulation of PMNs during inflammation.
Related Links	https://www.ahajournals.org/doi/pdf/10.1161/ATVBAHA.110.222208 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3548602/pdf https://www.ahajournals.org/doi/reader/10.1161/ATVBAHA.110.222208
Ending Page	1350
Page Count	9
Starting Page	1342
ISSN	10795642
e-ISSN	15244636
DOI	10.1161/atvbaha.110.222208
Journal	Arteriosclerosis, thrombosis, and vascular biology
Issue Number	6
Volume Number	31
Language	English
Publisher	Ovid Technologies (Wolters Kluwer Health)
Publisher Date	2011-06-01
Access Restriction	Open
Subject Keyword	Journal: Arteriosclerosis, thrombosis, and vascular biology Adhesion Molecules
Content Type	Text
Resource Type	Article
Subject	Cardiology and Cardiovascular Medicine

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