Cross-talk between minimally primed HL-60 cells and resting HUVEC reveals a crucial role for adhesion over extracellularly released oxidants.

Abstract:

: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. By exploring for the first time the potential for minimally primed neutrophil surrogates to induce endothelial dysfunction, this study suggests a novel mechanism which may be operative in pathologies, mediated by minimally primed neutrophils, such as hyperdyslipidemia and cardiovascular complications.

journal_name

Biochem Pharmacol

journal_title

Biochemical pharmacology

authors

Allegra M,D'Acquisto F,Tesoriere L,Livrea MA,Perretti M

doi

10.1016/j.bcp.2010.10.018

subject

Has Abstract

pub_date

2011-02-01 00:00:00

pages

396-401

issue

3

eissn

0006-2952

issn

1873-2968

pii

S0006-2952(10)00797-5

journal_volume

81

pub_type

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