PAF stimulates cAMP formation in P388D1 macrophage-like cells via the formation and secretion of prostaglandin E2 in an autocrine fashion

Reto Asmis; Edward A. Dennis

doi:10.1016/0167-4889(94)90203-8

PAF stimulates cAMP formation in P388D₁ macrophage-like cells via the formation and secretion of prostaglandin E₂ in an autocrine fashion

Reto Asmis, Edward A. Dennis

Department of Clinical Laboratory Sciences

Resultado de la investigación: Article › revisión exhaustiva

9 Citas (Scopus)

Resumen

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.

Idioma original	English (US)
Páginas (desde-hasta)	295-301
Número de páginas	7
Publicación	BBA - Molecular Cell Research
Volumen	1224
N.º	2
DOI	https://doi.org/10.1016/0167-4889(94)90203-8
Estado	Published - nov 10 1994

ASJC Scopus subject areas

Molecular Biology
Cell Biology

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10.1016/0167-4889(94)90203-8

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title = "PAF stimulates cAMP formation in P388D1 macrophage-like cells via the formation and secretion of prostaglandin E2 in an autocrine fashion",

abstract = "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.",

keywords = "Autocrine, Inositol 1,4,5-trisphosphate, Macrophage, Platelet activating factor, Prostaglandin E, cyclic AMP",

author = "Reto Asmis and Dennis, {Edward A.}",

note = "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.",

year = "1994",

month = nov,

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doi = "10.1016/0167-4889(94)90203-8",

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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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