Activation of protein kinase C inhibits prostaglandin- and potentiates adenosine receptor-stimulated accumulation of cyclic AMP in a human T-cell leukemia line.
Accumulation of cAMP in the human T-cell leukemia cell line Jurkat was stimulated by the adenosine analogue 5'-N-ethylcarboxamidoadenosine (NECA) and by prostaglandin E2 (PGE2). Addition of two phorbol esters, PDiBu and TPA, markedly enhanced the NECA-stimulated accumulation of cAMP whereas the PGE2-stimulated cAMP accumulation was substantially reduced. The non-tumor-promoting phorbol ester, 4 alpha-PDD, had no effect on either NECA- or PGE2-stimulated cAMP accumulation. The ability of PDiBu to inhibit the effect of PGE2 and to stimulate the effect of NECA remained in the presence a low concentration of forskolin (0.3 microM), which per se increased both NECA- and PGE2-stimulated cAMP accumulation. Our results suggest that the effect of PK-C-activating drugs on receptor-mediated cAMP accumulation is entirely dependent on which receptor is being stimulated.
D002460:Cell Line; D000242:Cyclic AMP / Q000378:metabolism*; D015232:Dinoprostone; D004789:Enzyme Activation; D006801:Humans; D007938:Leukemia / Q000201:enzymology* / Q000378:metabolism; D010703:Phorbol Esters / Q000494:pharmacology; D011458:Prostaglandins E / Q000494:pharmacology*; D011493:Protein Kinase C / Q000378:metabolism*; D011983:Receptors, Purinergic / Q000187:drug effects* / Q000502:physiology; D013601:T-Lymphocytes
D010703:Phorbol Esters; D011458:Prostaglandins E; D011983:Receptors, Purinergic; D000242:Cyclic AMP; D011493:Protein Kinase C; D015232:Dinoprostone