Forskolin and prostacyclin inhibit fluoride induced platelet activation and protein kinase C dependent responses.
Platelet activation (cytosolic [Ca2+] increase, aggregation and ATP secretion) was induced with A1F-4. This agent presumably interacts with a G protein which appears to mediate the coupling of the receptors for Ca mobilizing hormones and phospholipase C. All the A1F-4 evoked responses were inhibited by treatment with forskolin or prostacyclin, agents known to increase cellular cAMP. Thus the G protein-phospholipase C system appears to be the site of cAMP inhibition. Unexpectedly forskolin and prostacyclin also inhibited secretion and aggregation induced by the activators of protein kinase C, diglyceride and phorbol ester, suggesting that cAMP can also inhibit directly the protein kinase C dependent responses.
Doni
M G
MG
Department of Biological Chemistry, University of Padova, Italy.
Deana
R
R
Bertoncello
S
S
Zoccarato
F
F
Alexandre
A
A
D000255:Adenosine Triphosphate / Q000097:blood; D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism; D002118:Calcium / Q000097:blood; D005576:Colforsin / Q000494:pharmacology*; D000242:Cyclic AMP / Q000097:blood; D003600:Cytosol / Q000187:drug effects; D004789:Enzyme Activation / Q000187:drug effects; D011464:Epoprostenol / Q000494:pharmacology*; D005459:Fluorides / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D006801:Humans; D066298:In Vitro Techniques; D010972:Platelet Activating Factor / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D010974:Platelet Aggregation / Q000187:drug effects; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000097:blood*
D010972:Platelet Activating Factor; D005576:Colforsin; D000255:Adenosine Triphosphate; D011464:Epoprostenol; D000242:Cyclic AMP; D011493:Protein Kinase C; D005459:Fluorides; D002118:Calcium