Abstract：
:Leukotriene 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.
journal_name
J Cell Physioljournal_title
Journal of cellular physiologyauthors
Geirsson A,Halldórsson H,Magnúsdóttir K,Kjeld M,Thorgeirsson Gdoi
10.1002/(SICI)1097-4652(199810)177:1<103::AID-JCP1subject
Has Abstractpub_date
1998-10-01 00:00:00pages
103-8issue
1eissn
0021-9541issn
1097-4652pii
10.1002/(SICI)1097-4652(199810)177:1<103::AID-JCP1journal_volume
177pub_type
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