Activation of adenylate cyclase results in down-regulation of c-jun mRNA expression in rat C6 glioma cells

To investigate the possible mechanisms involved in forskolin-induced c-jun mRNA decrease in rat C6 glioma cells, we examined effects of a PKA inhibitor (H-89), a l-type Ca 2+ channel blocker (nimodipine), a calmodulin activation inhibitor (calmidazolium chloride) and a Ca 2+/calmodulin-dependent pro...

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Veröffentlicht in:Neuroscience letters 1999-11, Vol.276 (1), p.53-56
Hauptverfasser: Lee, Jin-Koo, Choi, Mi-Ran, Song, Dong-Keun, Huh, Sung-Oh, Kim, Yung-Hi, Suh, Hong-Won
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Sprache:eng
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Zusammenfassung:To investigate the possible mechanisms involved in forskolin-induced c-jun mRNA decrease in rat C6 glioma cells, we examined effects of a PKA inhibitor (H-89), a l-type Ca 2+ channel blocker (nimodipine), a calmodulin activation inhibitor (calmidazolium chloride) and a Ca 2+/calmodulin-dependent protein kinase II inhibitor (KN-62) on forskolin-induced c-jun mRNA down-regulation. H-89 caused a reversal of forskolin-induced c-jun mRNA decrease. Furthermore, nimodipine, KN-62 and calmidazolium chloride partially blocked forskolin-induced c-jun mRNA down-regulation. Our results suggest that activation of adenylate cyclase appears to be involved in a down-regulation of c-jun mRNA expression through a PKA pathway. In addition, l-type calcium channels, calmodulin and Ca 2+/calmodulin-dependent protein kinase II may be partially involved in c-jun mRNA down-regulation induced by forskolin.
ISSN:0304-3940
1872-7972
DOI:10.1016/S0304-3940(99)00780-6