TY - JOUR
T1 - PAF stimulates cAMP formation in P388D1 macrophage-like cells via the formation and secretion of prostaglandin E2 in an autocrine fashion
AU - Asmis, Reto
AU - Dennis, Edward A.
N1 - Funding Information:
We wish to thank Raymond Deems, Suzanne E. Barbour and Jesfis Balsinde for critical advice and for helpful suggestionsd uring the preparation of the manuscriptT. his work was supportedb y National Institutes of Health Research Grant HD26171. R.A. was supportedin part by the Swiss National Fund and the American Heart Association,C alifornia Affiliate Post-doctoralF ellowships.
PY - 1994/11/10
Y1 - 1994/11/10
N2 - The role of cAMP in the formation of prostaglandin E2 (PGE2) was investigated in bacterial lipopolysaccharide (LPS)-primed P388D1 macrophage-like cells stimulated with platelet activating factor (PAF). cAMP levels and PGE2 secretion were correlated with stimulation by PAF or ionomycin. Indomethacin inhibited cAMP formation induced by PAF, but not PGE2-stimulated cAMP production. Inositol (1,4,5)-trisphosphate levels were strongly reduced by exogenous PGE2 and increased by H-89, an inhibitor of PKA. However, exogenous PGE2 did not affect PAF-stimulated PGE2 formation. These results suggest that cAMP levels in P388D1 cells are regulated by PGE2 in an autocrine fashion. Evidence is presented that this feedback mechanism regulates inositol (1,4,5)-triphosphate levels in these cells, while PGE2 formation is not affected.
AB - The role of cAMP in the formation of prostaglandin E2 (PGE2) was investigated in bacterial lipopolysaccharide (LPS)-primed P388D1 macrophage-like cells stimulated with platelet activating factor (PAF). cAMP levels and PGE2 secretion were correlated with stimulation by PAF or ionomycin. Indomethacin inhibited cAMP formation induced by PAF, but not PGE2-stimulated cAMP production. Inositol (1,4,5)-trisphosphate levels were strongly reduced by exogenous PGE2 and increased by H-89, an inhibitor of PKA. However, exogenous PGE2 did not affect PAF-stimulated PGE2 formation. These results suggest that cAMP levels in P388D1 cells are regulated by PGE2 in an autocrine fashion. Evidence is presented that this feedback mechanism regulates inositol (1,4,5)-triphosphate levels in these cells, while PGE2 formation is not affected.
KW - Autocrine
KW - Inositol 1,4,5-trisphosphate
KW - Macrophage
KW - Platelet activating factor
KW - Prostaglandin E
KW - cyclic AMP
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U2 - 10.1016/0167-4889(94)90203-8
DO - 10.1016/0167-4889(94)90203-8
M3 - Article
C2 - 7981245
AN - SCOPUS:0028044218
SN - 0167-4889
VL - 1224
SP - 295
EP - 301
JO - Biochimica et Biophysica Acta - Molecular Cell Research
JF - Biochimica et Biophysica Acta - Molecular Cell Research
IS - 2
ER -