JPET Introducing ALZET?ew Model 2006 Pump

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Barzaghi, G.
Right arrow Articles by Mong, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Barzaghi, G.
Right arrow Articles by Mong, S.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*CALCIUM COMPOUNDS
*CALCIUM, ELEMENTAL

Platelet-activating factor-induced phosphoinositide metabolism in differentiated U-937 cells in culture

G Barzaghi, HM Sarau and S Mong

Laboratory for Cardiovascular Clinical Pharmacology, Instituto di Ricerche Farmacologiche Mario Negri, Milano, Italy.

Human monocytic leukemic U-937 cells, when differentiated with dimethylsulfoxide to macrophage-like state, express receptors for platelet-activating factor (PAF). In the differentiated U-937 cells, PAF induced hydrolysis of phosphoinositides and synthesis of inositol phosphates. PAF-induced production of inositol phosphates was rapid, concentration-dependent and was inhibited by a receptor antagonist CV3988, indicating that it was mediated via a specific receptor. In fura-2-loaded, differentiated U-937 cells, PAF induced immediate and concentration-dependent calcium mobilization [( Ca++]i) that was inhibited by CV3988, but not by calcium channel blockers. Addition of an increasing concentration of calcium chelator, ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid, to the medium inhibited a large fraction (approximately 75%) of PAF receptor-induced [Ca++]i mobilization thus suggesting the majority of [Ca++]i mobilization was originated from extracellular milieu and a small portion (approximately 25%) was originated from intracellular sources. The inositol phosphate production induced by PAF, however, was independent from the extracellular calcium and was not inhibited by the addition of ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid. Neither [Ca++]i mobilization or phosphoinositide metabolism in U- 937 cells was sensitive to treatment of pertussis toxin, but both types of effects were sensitive to treatment by an inhibitor of phospholipase C, manoalide. These results suggest that in differentiated U-937 cells PAF receptor is coupled through a pertussis toxin-insensitive guanine nucleotide binding protein to a phosphoinositide specific phospholipase C. Inositol-trisphosphate, and possibly diacylglycerol, could be the intracellular messengers for PAF receptor in U-937 cells.

Volume 248, Issue 2, pp. 559-566, 02/01/1989
Copyright © 1989 by American Society for Pharmacology and Experimental Therapeutics






Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
Molecular Interventions Drug Metabolism and Disposition

Copyright © 1989 by the American Society for Pharmacology and Experimental Therapeutics.