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Role of autocrine stimulation for the effects of cyclic AMP on protein and lipid phosphorylation in platelets activated by particles
Author(s) -
Ryningen Anita,
Holmsen Holm
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)01154-5
Subject(s) - forskolin , autocrine signalling , platelet activation , endocrinology , medicine , phosphorylation , platelet , tyrosine phosphorylation , chemistry , stimulation , receptor , biochemistry , biology
We have compared responses in platelets stimulated with the particulate materials, Intralipid (liposome‐suspension) and a potential contrast medium IEEC (1′‐(ethyloxycarbonyloxy)‐ethyl‐5‐acetyl‐amino‐3‐( N ‐methyl‐acetylamino)‐2,4,6‐triiodo‐benzenecarboxylate coated with human serum albumin), with and without forskolin and inhibitors of autocrine stimulation (IAS: an ADP‐removing system of creatine phosphate/creatine phosphokinase; RGDS to prevent fibrinogen/fibronectin binding to GPIIb/IIIa; SQ 29.548 as a TXA 2 receptor antagonist; cyproheptadine as a serotonin receptor antagonist; BN 52021 as a platelet‐activating factor receptor antagonist). The pattern of tyrosine‐phosphorylated proteins, phosphorylation of initial lipids and phosphorylation of pleckstrin (P47) were used as markers for early signal transducing responses, while secretion of ADP+ATP and β‐ N ‐acetyl‐glycosaminidase were used as final responses. Intralipid showed no platelet activation except for some weak tyrosine protein phosphorylation that was inhibited by elevated cAMP. IEEC induced strong platelet activation that was partly inhibited by increased levels of cAMP and IAS. The inhibition of elevated cAMP seemed to be due to removal of the G protein‐mediated activation from secreted autocrine stimulators either by IAS or forskolin. The remaining activity is a pure effect from IEEC which is not affected by elevated cAMP.