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Nicotine-induced phosphorylation of Akt through epidermal growth factor receptor and Src in PC12h cells.
- Source :
- Journal of Neurochemistry; 12/15/2002, Vol. 83 Issue 6, p1372-1379, 8p
- Publication Year :
- 2002
-
Abstract
- Nicotine treatment triggers calcium influx into neuronal cells, which promotes cell survival in a number of neuronal cells. Phosphoinositide (PI) 3-kinase and downstream PI3-kinase target Akt have been reported to be important in the calciummediated promotion of survival in a wide variety of cells. We investigated the mechanisms of nicotine-induced phosphorylation of Akt in PC12h cells, in comparison with nicotine-induced ERK phosphorylation. Nicotine induced Akt phosphorylation in a dose-dependent manner. A nicotinic acetylcholine receptor (nAChR) α7 subunit-selective inhibitor had no significant effect on nicotine-induced Akt phosphorylation, while a non-selective nAChR antagonist inhibited the phosphorylation. L-type voltage-sensitive calcium channel (VSCC) antagonists, calmodulin antagonist, and Ca[sup 2+]/calmudulin-dependent protein kinase (CaM kinase) inhibitor prevented the nicotine-induced Akt phosphorylation. Three epidermal growth factor receptor (EGFR) inhibitors prevented the nicotine-induced phosphorylation of both extracellular signal-regulated protein kinase (p42/ 44 MAP kinase, ERK) and Akt. In contrast, an inhibitor of the Src family tyrosine kinase prevented the nicotine-induced Akt phosphorylation but not ERK phosphorylation. These results suggested that nicotine induces the activation of both PI3kinase/Akt and ERK pathways via common pathways including non-α7-nAChRs, L-type VSCC, CaM kinase II and EGFR in PC12h cells, but Src family tyrosine kinases only participate in the pathway to activate Akt. [ABSTRACT FROM AUTHOR]
- Subjects :
- PHOSPHORYLATION
EPIDERMAL growth factor
Subjects
Details
- Language :
- English
- ISSN :
- 00223042
- Volume :
- 83
- Issue :
- 6
- Database :
- Complementary Index
- Journal :
- Journal of Neurochemistry
- Publication Type :
- Academic Journal
- Accession number :
- 8638815
- Full Text :
- https://doi.org/10.1046/j.1471-4159.2002.01248.x