Title : Nitric oxide promotes nicotine-triggered ERK signaling via redox reactions in PC12 cells.

Pub. Date : 2011 Oct 30

PMID : 21742048






7 Functional Relationships(s)
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1 In the present study, we demonstrated that nNOS expression enhances the nicotine-triggered activation of extracellular signal-regulated kinase 1/2 (ERK1/2) in nNOS-transfected PC12 (NPC12) cells. Nicotine mitogen activated protein kinase 3 Rattus norvegicus
2 In the present study, we demonstrated that nNOS expression enhances the nicotine-triggered activation of extracellular signal-regulated kinase 1/2 (ERK1/2) in nNOS-transfected PC12 (NPC12) cells. Nicotine mitogen activated protein kinase 3 Rattus norvegicus
3 Treatment with nicotine increased the phosphorylation level of ERK1/2 in the NPC12 cells as compared with that in control PC12 cells. Nicotine mitogen activated protein kinase 3 Rattus norvegicus
4 The nicotine-induced ERK1/2 phosphorylation in PC12 cells was observed by their pretreatment with a NO donor. Nicotine mitogen activated protein kinase 3 Rattus norvegicus
5 Moreover, the enhancement of nicotine-induced ERK1/2 phosphorylation in the NPC12 cells was regulated by intracellular glutathione levels, but not by the soluble guanylate cyclase-cGMP-protein kinase G signaling. Nicotine mitogen activated protein kinase 3 Rattus norvegicus
6 Taken together, these findings suggest that nicotine modulates NO-dependent redox condition; the resulting calcium influx, would increase ERK1/2 phosphorylation in nNOS expressing cells. Nicotine mitogen activated protein kinase 3 Rattus norvegicus
7 Blockade of NO pathway may be selective target to reduce ERK1/2 phosphorylation via attenuation of the nicotine responses in the CNS. Nicotine mitogen activated protein kinase 3 Rattus norvegicus