Title : Chronic nicotine exposure enhances insulin-induced mitogenic signaling via up-regulation of alpha7 nicotinic receptors in isolated rat aortic smooth muscle cells.

Pub. Date : 2007 Feb

PMID : 17068140






6 Functional Relationships(s)
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1 Short-term nicotine treatment stimulated phosphorylation of p44/42-MAPK, p38-MAPK, and signal transducer and activator of transcription 3. Nicotine mitogen activated protein kinase 3 Rattus norvegicus
2 However, an additive effect of nicotine pretreatment on insulin stimulation was only observed on p44/42-MAPK. Nicotine mitogen activated protein kinase 3 Rattus norvegicus
3 The nicotine-induced phosphorylation of p44/42-MAPK and [methyl-(3)H]thymidine incorporation were effectively suppressed by a alpha7-nAChR-selective antagonist, methyllycaconitine, and the phosphorylation of p44/42-MAPK was stimulated by a alpha7-nAChR-specific agonist, GTS21. Nicotine mitogen activated protein kinase 3 Rattus norvegicus
4 The nicotine-induced phosphorylation of p44/42-MAPK and [methyl-(3)H]thymidine incorporation were effectively suppressed by a alpha7-nAChR-selective antagonist, methyllycaconitine, and the phosphorylation of p44/42-MAPK was stimulated by a alpha7-nAChR-specific agonist, GTS21. Nicotine mitogen activated protein kinase 3 Rattus norvegicus
5 Interestingly, long-term (48-h) pretreatment with nicotine increased the amount of alpha7-AChR in the plasma membrane and insulin-induced phosphorylation of p44/42-MAPK. Nicotine mitogen activated protein kinase 3 Rattus norvegicus
6 These results provide the first evidence that acute exposure to nicotine enhances insulin-induced mitogenesis predominantly by affecting the phosphorylation of p44/42-MAPK and that chronic exposure further augments the insulin signal via up-regulation of alpha7-nAChR, which may be crucial for the development and progression of atherosclerosis in large vessels. Nicotine mitogen activated protein kinase 3 Rattus norvegicus