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Volume 220, Issue 1 p. 57-60
Full-length article
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Activation of protein kinase C inhibits prostaglandin- and potentiates adenosine receptor-stimulated accumulation of cyclic AMP in a human T-cell leukemia line

Christer Nordstedt

Christer Nordstedt

Department of Pharmacology, Karolinska Institutet, Box 60400, S-104 01 Stockholm, Sweden

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Mikael Jondal

Mikael Jondal

Department of Immunology, Karolinska Institutet, Box 60400, S-104 01 Stockholm, Sweden

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Bertil B. Fredholm

Bertil B. Fredholm

Department of Pharmacology, Karolinska Institutet, Box 60400, S-104 01 Stockholm, Sweden

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First published: August 10, 1987
Citations: 22

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