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Quantum dots reveal endothelial NOX2 induces VCAM expression in LPS‐challenged inflamed whole lung (855.2)
Author(s) -
Orndorff Rebecca,
Hong Nan Kang,
Yu Kevin,
Zern Blaine,
Feinstein Sheldon,
Fisher Aron,
Muzykantov Vladimir,
Chatterjee Shampa
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.855.2
Subject(s) - vcam 1 , nadph oxidase , apocynin , inflammation , endothelium , in vivo , cell adhesion molecule , microbiology and biotechnology , icam 1 , biology , reactive oxygen species , immunology , chemistry , endocrinology
Quantum Dot (QD) technology coupled with fluorescence imaging is a powerful tool to detect cellular proteins in vivo. Here we employ QDs as an imaging tool to detect vascular cell adhesion molecule‐1 (VCAM) expression in a model of lung inflammation. A key event in inflammation is the expression of VCAM. VCAM induction is reportedly responsible for the accumulation of neutrophils in lungs and for subsequent production of reactive oxygen species (ROS). NADPH oxidase 2 (NOX2), expressed by both endothelial cells and neutrophils, is a major contributor to ROS production post inflammation in the lungs. To date, the cellular sources of NOX2 (neutrophils or endothelium) that regulate VCAM expression in inflamed lungs is unknown. Using QD probes specific for VCAM, we found increased VCAM expression post LPS‐challenge in vitro, which was abrogated by the NOX2 inhibitor, apocynin. Ex vivo and in vivo lungs exhibited an 8‐10 fold higher incidence of VCAM expression in LPS‐challenged lungs over NOX2 null lungs. We next employed an endothelial specific NOX2 expressing transgenic mouse in a NOX2 null background (endoNOX2Tg) to reveal that endothelial NOX2 induces VCAM expression at levels that are intermediate between those expressed in wild‐type (WT) and NOX2 null mice. This result indicates that endothelial NOX2 is sufficient to induce VCAM expression due to an inflammatory stimulus. Grant Funding Source : Supported by T32‐HL07748.