Stimulation of muscarinic receptors induces expression of individual fos and jun genes through different transduction pathways
(1998) In Journal of Neurochemistry 70(4). p.1722-1729- Abstract
- The transduction pathways coupling muscarinic receptors to induction of fos and jun genes were investigated in neuroblastoma SH-SY5Y cells. Stimulation with carbachol induced expression of c-fos, fosB, c-jun, junB, and junD. This effect was abolished by pretreatment with atropine, indicating an involvement of muscarinic receptors. These genes were also induced by activation of protein kinase C with phorbol ester or by elevating the intracellular Ca2+ concentration with a Ca2+ ionophore. The Ca2+ effect was inhibited by KN-62, suggesting an induction through Ca2+/calmodulin-dependent kinase II. Inhibition of protein kinase C with GF109203X suppressed the carbachol-stimulated increase in mRNA levels of c-fos, fosB, and junB by approximately... (More)
- The transduction pathways coupling muscarinic receptors to induction of fos and jun genes were investigated in neuroblastoma SH-SY5Y cells. Stimulation with carbachol induced expression of c-fos, fosB, c-jun, junB, and junD. This effect was abolished by pretreatment with atropine, indicating an involvement of muscarinic receptors. These genes were also induced by activation of protein kinase C with phorbol ester or by elevating the intracellular Ca2+ concentration with a Ca2+ ionophore. The Ca2+ effect was inhibited by KN-62, suggesting an induction through Ca2+/calmodulin-dependent kinase II. Inhibition of protein kinase C with GF109203X suppressed the carbachol-stimulated increase in mRNA levels of c-fos, fosB, and junB by approximately 70% but had only minor effects on the expression of c-jun and junD. On the other hand, preincubation with KN-62 attenuated the carbachol-induced increase in c-jun and junD expression by 70% but had no effect on c-fos, fosB, and junB mRNA levels. Simultaneous inhibition of both protein kinase C and Ca2+/calmodulin-dependent kinase II completely abolished the carbachol-stimulated expression of c-jun and junD, but c-fos, fosB, and junB were still expressed to a certain extent under this condition. Comparison of the inhibitory effects of GF109203X and Go 6976 suggests the involvement of classical protein kinase C isozymes in muscarinic receptor-stimulated expression of fos and jun genes. These results demonstrate that the muscarinic receptor-induced expression of individual fos and jun genes is regulated via different pathways, primarily protein kinase C or Ca2+/calmodulin-dependent kinase II. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1112630
- author
- Ding, Wei-Qun ; Larsson, Christer LU and Alling, Christer LU
- organization
- publishing date
- 1998
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Muscarinic receptor, Protein kinase C, Immediate-early genes, SH-SY5Y neuroblastoma cells, Ca2+/calmodulin-dependent kinase II
- in
- Journal of Neurochemistry
- volume
- 70
- issue
- 4
- pages
- 1722 - 1729
- publisher
- Wiley-Blackwell
- external identifiers
-
- pmid:9523591
- scopus:0031881692
- ISSN
- 1471-4159
- DOI
- 10.1046/j.1471-4159.1998.70041722.x
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Division of Clinical Chemistry and Pharmacology (013250300), Tumour Cell Biology (013017530)
- id
- daf2abd2-2c23-4560-a0bf-93275d780437 (old id 1112630)
- date added to LUP
- 2016-04-01 16:19:14
- date last changed
- 2022-01-28 18:50:29
@article{daf2abd2-2c23-4560-a0bf-93275d780437,
abstract = {{The transduction pathways coupling muscarinic receptors to induction of fos and jun genes were investigated in neuroblastoma SH-SY5Y cells. Stimulation with carbachol induced expression of c-fos, fosB, c-jun, junB, and junD. This effect was abolished by pretreatment with atropine, indicating an involvement of muscarinic receptors. These genes were also induced by activation of protein kinase C with phorbol ester or by elevating the intracellular Ca2+ concentration with a Ca2+ ionophore. The Ca2+ effect was inhibited by KN-62, suggesting an induction through Ca2+/calmodulin-dependent kinase II. Inhibition of protein kinase C with GF109203X suppressed the carbachol-stimulated increase in mRNA levels of c-fos, fosB, and junB by approximately 70% but had only minor effects on the expression of c-jun and junD. On the other hand, preincubation with KN-62 attenuated the carbachol-induced increase in c-jun and junD expression by 70% but had no effect on c-fos, fosB, and junB mRNA levels. Simultaneous inhibition of both protein kinase C and Ca2+/calmodulin-dependent kinase II completely abolished the carbachol-stimulated expression of c-jun and junD, but c-fos, fosB, and junB were still expressed to a certain extent under this condition. Comparison of the inhibitory effects of GF109203X and Go 6976 suggests the involvement of classical protein kinase C isozymes in muscarinic receptor-stimulated expression of fos and jun genes. These results demonstrate that the muscarinic receptor-induced expression of individual fos and jun genes is regulated via different pathways, primarily protein kinase C or Ca2+/calmodulin-dependent kinase II.}},
author = {{Ding, Wei-Qun and Larsson, Christer and Alling, Christer}},
issn = {{1471-4159}},
keywords = {{Muscarinic receptor; Protein kinase C; Immediate-early genes; SH-SY5Y neuroblastoma cells; Ca2+/calmodulin-dependent kinase II}},
language = {{eng}},
number = {{4}},
pages = {{1722--1729}},
publisher = {{Wiley-Blackwell}},
series = {{Journal of Neurochemistry}},
title = {{Stimulation of muscarinic receptors induces expression of individual fos and jun genes through different transduction pathways}},
url = {{http://dx.doi.org/10.1046/j.1471-4159.1998.70041722.x}},
doi = {{10.1046/j.1471-4159.1998.70041722.x}},
volume = {{70}},
year = {{1998}},
}