Cross-talk between minimally-primed HL-60 cells and resting HUVEC reveals a crucial role for adhesion over extracellularly-released oxidants.
Résumé
This study demonstrates that a long-lasting co-culture of neutrophil surrogates (HL-60 cells), minimally-primed by platelet activating factor (PAF), and resting endothelial cells (EC) results in the elaboration of an hyper-adhesive endothelial surface, as measured by the increase in the expression of endothelial adhesion molecules E-Selectin, VCAM-1, and ICAM-1. This endothelial dysfunction is mediated by the activation of the redox-sensitive transcription factor NF-κB through an exclusive adhesion-driven mechanism active in the endothelial cell: reactive oxygen and nitrogen species, extracellularly-released by minimally-primed HL-60 cells, are not involved in the induction of the endothelial dysfunction.
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