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

Abstract

To cite this version:M. Allegra, F.D'Acquisto, L. Tesoriere, M.A. Livrea, M. Perretti. Cross-talk between minimallyprimed HL-60 cells and resting HUVEC reveals a crucial role for adhesion over extracellularly-released oxidants.. Biochemical Pharmacology, Elsevier, 2010, 81 (3) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 2 AbstractThis 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-B through an exclusive adhesion-driven mechanism active in the endothelial cell: reactive oxygen and nitrogen species, extracellularly-released by minimallyprimed 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.

Indicaxanthin from Opuntia ficus indica (L. Mill) Inhibits Oxidized LDL-Mediated Human Endothelial Cell Dysfunction through Inhibition of NF-κB Activation

“…It is well established that endothelial adhesion molecule expression is under control of several redox-regulated transcription factors, including the master minder NF- κ B [20]. Moreover, oxLDL have been demonstrated to activate various transcription factors, NF- κ B included.…”