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

FEBS Lett. 1987 Aug 10;220(1):57-60. doi: 10.1016/0014-5793(87)80875-x.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line
  • Cyclic AMP / metabolism*
  • Dinoprostone
  • Enzyme Activation
  • Humans
  • Leukemia / enzymology*
  • Leukemia / metabolism
  • Phorbol Esters / pharmacology
  • Prostaglandins E / pharmacology*
  • Protein Kinase C / metabolism*
  • Receptors, Purinergic / drug effects*
  • Receptors, Purinergic / physiology
  • T-Lymphocytes


  • Phorbol Esters
  • Prostaglandins E
  • Receptors, Purinergic
  • Cyclic AMP
  • Protein Kinase C
  • Dinoprostone