Title : Nicotine stimulates IL-6 expression by activating the AP-1 and STAT-3 pathways in human endothelial EA.hy926 cells.

Pub. Date : 2019 Apr

PMID : 30317657






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1 Nicotine stimulates IL-6 expression by activating the AP-1 and STAT-3 pathways in human endothelial EA.hy926 cells. Nicotine interleukin 6 Homo sapiens
2 In this study, we investigated the effects of nicotine, a major psychoactive compound in cigarette smoke, on IL-6 expression and EA.hy926 endothelial cell invasion. Nicotine interleukin 6 Homo sapiens
3 Nicotine stimulated IL-6 expression via the activator protein 1 (AP-1) transcription factor. Nicotine interleukin 6 Homo sapiens
4 Pharmacological inhibition and mutagenesis studies indicated that p38 mitogen-activated protein kinase (MAPK) mediated the IL-6-induced upregulation of nicotine in EA.hy926 cells. Nicotine interleukin 6 Homo sapiens
5 Furthermore, the antioxidant compound N-acetyl-cysteine eliminated the nicotine-activated production of reactive oxygen species (ROS) and inhibited signal transducer and activator of transcription 3 (STAT-3) phosphorylation; these two mechanisms mediated the upregulation of IL-6 expression by nicotine. Nicotine interleukin 6 Homo sapiens
6 In addition, the EA.hy926 cells treated with nicotine displayed markedly enhanced invasiveness due to IL-6 upregulation. Nicotine interleukin 6 Homo sapiens
7 Our data demonstrate that nicotine induced IL-6 expression, which, in turn, enhanced the invasiveness of endothelial EA.hy926 cells, via activation of the p38 MAPK/AP-1 and ROS/STAT-3 signaling pathways. Nicotine interleukin 6 Homo sapiens