Activation of protein kinase C inhibits prostaglandin‐ and potentiates adenosine receptor‐stimulated accumulation of cyclic AMP in a human T‐cell leukemia line

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Abstract
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, 4α‐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 μM), 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

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