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PMID: 2555306 Published · ppublish English Journal Article

Cyclic AMP inhibits chemotactic-peptide-induced but not Ca2+-ionophore- or tetradecanoylphorbol-acetate-induced enzyme secretion in guinea pig neutrophils.

International archives of allergy and applied immunology ·Vol. 90 ·No. 2 ·1989-00-00 ·Pages 194-7

Wada Y

Abstract

cAMP-increasing agents such as prostaglandin El, dibutyryl cAMP and 8-bromo-cAMP inhibited N-acetyl-beta-D-glucosaminidase secretion induced by the chemotactic peptide formylmethionyl-leucyl-phenylalanine in guinea pig neutrophils. However, they could not inhibit but rather potentiated the secretion significantly when secretion was induced by the Ca2+ ionophore A23187. Similarly, these agents did not inhibit tetradecanoylphorbol acetate (TPA)-induced secretion. Moreover, the secretion induced by combined treatment with Ca2+ ionophore A23187 and TPA was hardly blocked by cAMP-increasing agents. These results strongly suggest that cAMP inhibits the secretion through suppression of a signal transduction from receptor activation to events such as Ca2+ mobilization and protein kinase C activation, probably of the inositol phospholipid metabolism.

MeSH Terms
8-Bromo Cyclic Adenosine Monophosphate/pharmacology Alprostadil/pharmacology Animals Bucladesine/pharmacology Calcimycin/pharmacology Cyclic AMP/pharmacology Guinea Pigs N-Formylmethionine Leucyl-Phenylalanine/pharmacology Neutrophils/drug effects,enzymology Signal Transduction/drug effects Tetradecanoylphorbol Acetate/pharmacology
Chemicals
8-Bromo Cyclic Adenosine Monophosphate Calcimycin N-Formylmethionine Leucyl-Phenylalanine Bucladesine Cyclic AMP Alprostadil Tetradecanoylphorbol Acetate
Authors & Affiliations
1 authors, click to expand affiliations / ORCID
Wada Y
Research Laboratories, Shionogi & Co., Ltd., Osaka, Japan.
Article Info
Journal
International archives of allergy and applied immunology
Abbr.
Int Arch Allergy Appl Immunol
ISSN
0020-5915
Published
1989-00-00
Pages
194-7
Language
English
Region
Switzerland
NLM ID
0404561
Subset
IM
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