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PAF effects on transmembrane signaling pathways in rat kupffer cells.
- Source :
- Lipids; Dec1991, Vol. 26 Issue 12, p1038-1043, 6p
- Publication Year :
- 1991
-
Abstract
- Platelet activating factor (PAF) was found to stimulate the metabolism of inositol phospholipids via deacylation and phospholipase C in Kupffer cells, the resident macrophages in liver. PAF-induced phosphoinositide metabolism occurred in two phases. Within seconds after stimulation, in the absence of extracellular Ca, platelet activating factor caused the phosphodiester hydrolysis of phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 4-phosphate with the release of inositol 1,4,5-trisphosphate and inositol 1,4-bisphosphate. This was followed by an extracellular Ca-dependent release of glycerophosphoinositol, inositol monophosphates and inositol bisphosphates. Various Ca-mobilizing agonists failed to evoke hydrolysis of phosphoinositides. Platelet activating factor also stimulated the synthesis and release of prostaglandins from these cells. Platelet activating factor-stimulated phosphodiester metabolism of phosphoinositides and prostaglandin synthesis was inhibited by treatment with pertussis toxin and cholera toxin. Pertussis toxin also inhibited platelet activating factor-induced glycerophosphoinositol release. Cholera toxin, in contrast, stimulated platelet activating factor-induced glycerophosphoinositol release and prostaglandin synthesis and synergistically stimulated the effect of platelet activating factor on these processes. The results suggest that platelet activating factor-induced metabolism in the Kupffer cells occurs via specific receptors and may be mediated through the activation of different G-proteins. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 00244201
- Volume :
- 26
- Issue :
- 12
- Database :
- Complementary Index
- Journal :
- Lipids
- Publication Type :
- Academic Journal
- Accession number :
- 72269943
- Full Text :
- https://doi.org/10.1007/BF02536498