12-o-retinoylphorbol-13-acetate has been researched along with Glioma* in 2 studies
2 other study(ies) available for 12-o-retinoylphorbol-13-acetate and Glioma
| Article | Year |
|---|---|
Alpha2 adrenoreceptor agonist regulates protein kinase C-induced heat shock protein 27 phosphorylation in C6 glioma cells.
Dexmedetomidine (Dexmd), a potent and highly specific alpha(2) adrenoreceptor agonist, is an efficient therapeutic agent for sedation. Dexmd has been recently reported to have a neuroprotective effect. Heat shock protein (HSP) 27, a low-molecular weight HSP has been shown to be expressed following cerebral ischemia in astrocytes but not in neurons. HSP27 expression is involved in ischemic tolerance of the brain. This study investigated the effect of Dexmd on HSP27 in rat C6 glioma cells. 12-O-tetradecanoylphorbol-13-actate (TPA), a direct activator of protein kinase C (PKC), stimulated the phosphorylation of HSP27 at Ser82, but not Ser15 in a time-dependent manner. Prostaglandin (PG) E(1) or PGE(2) which activates the adenylyl cyclase-cAMP system as well as forskolin and dibutyryl-cAMP, suppressed the TPA-induced phosphorylation of HSP27. Dexmd reversed the suppression of HSP27 phosphorylation by the adenylyl cyclase-cAMP system. Therefore, these results strongly suggest that Dexmd reverses the suppression of HSP27 phosphorylation by the adenylyl cyclase-cAMP system activation through the inhibition of its system in C6 cells. alpha(2) Adrenoreceptor agonists may therefore show a neuroprotective effect through the modification of HSP27 phosphorylation induced by PKC activation. Topics: Adrenergic alpha-Agonists; Alprostadil; Analysis of Variance; Animals; Bucladesine; Cell Line, Tumor; Colforsin; Cyclic AMP; Dexmedetomidine; Dinoprostone; Drug Interactions; Gene Expression Regulation, Neoplastic; Glioma; Heat-Shock Proteins; Phorbol Esters; Phosphorylation; Protein Kinase C; Rats; Serine; Time Factors | 2008 |
Second stage tumor promoters: differences in biological potency and phorbol ester receptor affinity in C6 cells.
We have shown that the second stage tumor promoters mezerein (MEZ) and phorbol 12-retinoate 13-acetate (PRA) inhibit the gluccocorticoid-induced increase in glycerol phosphate dehydrogenase (GPDH) activity in C6 rat glioma cells with ED 50-values of 3.9 and 2.9 nM, respectively. Phorbol 12-myristate 13-acetate (PMA) was 10-fold less potent. MEZ was likewise more potent than PMA for inhibition of cAMP formation in response to isoproterenol. Binding competition studies using [3H]phorbol 12,13-dibutyrate ([3H]PDBu) yielded apparent Ki-values for MEZ and PRA of 50-70 nM. The large difference between the biological potencies of MEZ and PRA and their affinity for the major phorbol ester receptor suggest they may be acting through a more complicated mechanism in these cells. Topics: Animals; Caenorhabditis elegans Proteins; Carcinogens; Carrier Proteins; Cell Line; Cyclic AMP; Diterpenes; Glioma; Glycerolphosphate Dehydrogenase; Phorbol 12,13-Dibutyrate; Phorbol Esters; Protein Kinase C; Rats; Receptors, Drug; Receptors, Immunologic; Terpenes; Tetradecanoylphorbol Acetate | 1987 |