Potentiating effects of pertussis toxin on leukotriene C4 induced formation of inositol phosphate and prostacyclin in human umbilical vein endothelial cells.
Cast your vote
You can rate an item by clicking the amount of stars they wish to award to this item.
When enough users have cast their vote on this item, the average rating will also be shown.
Your vote was cast
Thank you for your feedback
Thank you for your feedback
MetadataShow full item record
CitationJ. Cell. Physiol. 1998, 177(1):103-8
AbstractLeukotriene C4 is an arachidonic acid metabolite and an important mediator of inflammation and anaphylaxis that is known to induce production of prostacyclin in endothelial cells. The goal of this study was to examine the signal transduction mechanisms activated by leukotriene C4 stimulation. Formation of inositol phosphates was measured to determine the activation of phospholipase C and pertussis toxin was used to explore the role of G-proteins. Additionally, we evaluated the role of protein kinase C in these events, especially whether there was an interaction between pertussis toxin mediated effects and the activity of protein kinase C. Leukotriene C4 induced a dose- and time-dependent formation of inositol phosphates and prostacyclin. The response to leukotriene C4 was greater than the response to leukotriene D4 even after treatment with L-serine borate complex, suggesting the presence of a specific leukotriene C4 receptor. Exposure to pertussis toxin potentiated, time-dependently, the leukotriene C4 induced formation of inositol phosphates and prostacyclin through a mechanism which was altered by manipulation of protein kinase C activity. The exact mechanism is not clear but our results are consistent with a postulated dual mechanism of phospholipase C control, in which leukotriene C4 induced stimulation is attenuated by a pertussis toxin sensitive G-protein.
DescriptionTo access publisher full text version of this article. Please click on the hyperlink in Additional Links field
- Endothelial inositol phosphate generation and prostacyclin production in response to G-protein activation by AlF4-.
- Authors: Magnússon MK, Halldórsson H, Kjeld M, Thorgeirsson G
- Issue date: 1989 Dec 15
- Trypanosoma cruzi: infection of cultured human endothelial cells alters inositol phosphate synthesis.
- Authors: Morris SA, Bilezikian JP, Hatcher V, Weiss LM, Tanowitz HB, Wittner M
- Issue date: 1989 Nov
- Flow-induced prostacyclin production is mediated by a pertussis toxin-sensitive G protein.
- Authors: Berthiaume F, Frangos JA
- Issue date: 1992 Aug 24
- Dual role of GTP-binding proteins in the control of endothelial prostacyclin.
- Authors: Pirotton S, Erneux C, Boeynaems JM
- Issue date: 1987 Sep 30
- Islet-activating protein inhibits leukotriene D4- and leukotriene C4- but not bradykinin- or calcium ionophore-induced prostacyclin synthesis in bovine endothelial cells.
- Authors: Clark MA, Conway TM, Bennett CF, Crooke ST, Stadel JM
- Issue date: 1986 Oct