Title : Nicotine enhances human vascular endothelial cell expression of ICAM-1 and VCAM-1 via protein kinase C, p38 mitogen-activated protein kinase, NF-kappaB, and AP-1.

Pub. Date : 2006

PMID : 16845181






6 Functional Relationships(s)
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1 Nicotine enhances human vascular endothelial cell expression of ICAM-1 and VCAM-1 via protein kinase C, p38 mitogen-activated protein kinase, NF-kappaB, and AP-1. Nicotine vascular cell adhesion molecule 1 Homo sapiens
2 The aim of this study was to determine the effect of nicotine on the expression of the adhesion molecules, intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 in endothelial cells and to determine the involvement of important known intermediaries, protein kinase C (PKC), p38 mitogen-activated protein kinase (p38 MAPK), and the transcription factors NF-kappaB and AP-1. Nicotine vascular cell adhesion molecule 1 Homo sapiens
3 We observed that nicotine increased the expression of ICAM-1 and VCAM-1 with a peak at 6 h. p38 MAPK was activated after 5 min exposure to 10-8 mol/L nicotine and returned to baseline levels by 30 min. Nicotine vascular cell adhesion molecule 1 Homo sapiens
4 We observed that nicotine increased the expression of ICAM-1 and VCAM-1 with a peak at 6 h. p38 MAPK was activated after 5 min exposure to 10-8 mol/L nicotine and returned to baseline levels by 30 min. Nicotine vascular cell adhesion molecule 1 Homo sapiens
5 Inhibitors of p38 MAPK, PKC, and NF-kappaB suppressed nicotine-stimulated expression of ICAM-1 and VCAM-1. Nicotine vascular cell adhesion molecule 1 Homo sapiens
6 Our results indicate that nicotine enhances the expression of ICAM-1 and VCAM-1 on the endothelial cell surface via a second messenger pathway which involves PKC and p38 MAPK-mediated activation of NF-kappaB and AP-1, resulting in increased expression of these cellular adhesion molecules. Nicotine vascular cell adhesion molecule 1 Homo sapiens