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Am J Physiol Renal Physiol 283: F944-F951, 2002. First published July 9, 2002; doi:10.1152/ajprenal.00072.2002
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Vol. 283, Issue 5, F944-F951, November 2002

Phospholipid metabolite production in human urothelial cells after protease-activated receptor cleavage

Alice Rickard and Jane McHowat

Department of Pathology, St. Louis University School of Medicine, St. Louis, Missouri 63104

Our laboratory demonstrated previously that stimulation of protease-activated receptors (PARs) on the human urothelial carcinoma cell line RT4 results in activation of a calcium-independent phospholipase A2 (iPLA2), leading to arachidonic acid and PGE2 release. In this study, we have examined PAR activation in normal human urothelial cells (HUR) leading to the production of inflammatory or cytoprotective phospholipid metabolites. The presence of both PAR-1 and PAR-2 on HUR was confirmed by immunoblotting. Stimulation of PAR-1 with thrombin or PAR-2 by tryptase leads to activation of a membrane-associated iPLA2 and the production of platelet-activating factor, arachidonic acid, and PGE2. These responses were all blocked by pretreatment with the iPLA2-selective inhibitor bromoenol lactone. Thus stimulation of PAR-1 or PAR-2 on HUR leads to iPLA2-catalyzed phospholipid hydrolysis, resulting in the production of metabolites that may mediate inflammation or provide cytoprotection to the bladder.

thrombin; tryptase; bromoenol lactone


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