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

[摘要]

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

[学科分类] 生物化学/生物物理

[关键词] Lymphocyte;Phorbol ester;Phosphorylation;Adenylate cyclase;Forskolin;CAMP;cyclic adenosine 3′;5′-monophosphate;PDiBu;β-phorbol-12;13-dibutyrate;TPA;12-O-tetradecanoyl phorbol 13-acetate;4α-PDD;4α-phorbol 12;13-didecanoate;NECA;N-ethyl-5′-carboxamidoadenosine;PGE2;prostaglandin E2;PK-C;protein kinase C;PCA;perchloric acid