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Am J Physiol Renal Physiol (July 9, 2002). doi:10.1152/ajprenal.00072.2002
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Articles in PresS, published online ahead of print July 9, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00072.2002
Submitted on February 19, 2002
Accepted on December 31, 1969

Production of Phospholipid Metabolites Following Cleavage of Protease-Activated Receptors on Human Urothelial Cells

Alice Rickard1 and Jane McHowat1*

1 Department of Pathology, Saint Louis University School of Medicine, St. Louis, MO, USA

* To whom correspondence should be addressed. E-mail: mchowatj{at}slucare1.sluh.edu.

We have demonstrated previously that stimulation of protease-activated receptors (PAR) on the human urothelial carcinoma cell line RT4 results in activation of a calcium-independent phospholipase A2 (iPLA2), leading to arachidonic acid and prostaglandin E2 (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, calcium-independent phospholipase A2 (iPLA2) and the production of platelet-activating factor (PAF), arachidonic acid and prostaglandin E2 (PGE2). These responses were all blocked by pretreatment with the iPLA2-selective inhibitor bromoenol lactone (BEL). 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.




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