Abstract
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 Ca2+ channel blocker (nimodipine), a calmodulin activation inhibitor (calmidazolium chloride) and a Ca2+/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 Ca2+/calmodulin-dependent protein kinase II may be partially involved in c-jun mRNA down-regulation induced by forskolin.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / analogs & derivatives
-
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / pharmacology
-
Adenylyl Cyclases / metabolism*
-
Animals
-
Calcium Channel Blockers / pharmacology
-
Calmodulin / antagonists & inhibitors
-
Colforsin / pharmacology
-
Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors
-
Down-Regulation / physiology*
-
Enzyme Activation / physiology
-
Enzyme Inhibitors / pharmacology
-
Glioma / metabolism*
-
Glioma / pathology
-
Imidazoles / pharmacology
-
Isoquinolines / pharmacology
-
Nimodipine / pharmacology
-
Proto-Oncogene Proteins c-jun / genetics*
-
RNA, Messenger / metabolism*
-
Rats
-
Sulfonamides*
-
Tumor Cells, Cultured
Substances
-
Calcium Channel Blockers
-
Calmodulin
-
Enzyme Inhibitors
-
Imidazoles
-
Isoquinolines
-
Proto-Oncogene Proteins c-jun
-
RNA, Messenger
-
Sulfonamides
-
Colforsin
-
calmidazolium
-
Nimodipine
-
KN 62
-
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
-
Cyclic AMP-Dependent Protein Kinases
-
Adenylyl Cyclases
-
N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide