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

FEBS Letters

Jondal, Mikael¹  Fredholm, Bertil B.²  Nordstedt, Christer² 

[1] Department of Immunology, Karolinska Institutet, Box 60400, S-104 01 Stockholm, Sweden;Department of Pharmacology, Karolinska Institutet, Box 60400, S-104 01 Stockholm, Sweden

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;   

DOI  :  10.1016/0014-5793(87)80875-X

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 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

【 授权许可】

Unknown