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Loss of prostaglandin E₂ release from immortalized urothelial cells obtained from interstitial cystitis patient bladders

¹Department of Pathology, Saint Louis University School of Medicine, St. Louis, Missouri; and ²Department of Urology, Northwestern University Feinberg School of Medicine, Chicago, Illinois

Submitted 2 December 2007 ; accepted in final form 4 March 2008

Interstitial cystitis (IC) is associated with increased activated mast cell numbers in the bladder and impairment of the barrier function of the urothelium. We stimulated immortalized urothelial cells derived from the inflamed region of IC bladders (SR22A or SM28 abn) or from healthy bladders (PD07i or PD08i) with tryptase and measured phospholipase A₂ (PLA₂) activity and the resultant release of arachidonic acid and prostaglandin E₂ (PGE₂). Tryptase stimulation of either PD07i or SR22A resulted in similar increases in PLA₂ activity and arachidonic acid release. However, tryptase stimulation of SR22A and SM28 abn did not result in a significant increase in PGE₂ release compared with the increase in PGE₂ release from tryptase-stimulated PD07i and PD08i cells. Expression of mRNA for cyclooxygenase-2 and PGE synthase was lower and mRNA for 15-hydroxyprostaglandin dehydrogenase was higher in SR22A compared with PD07i, suggesting that both decreased synthesis and increased metabolism are responsible for the lack of a PGE₂ response in tryptase-stimulated SR22A cells. Since PGE₂ is a cytoprotective eicosanoid, the failure to produce this metabolite in cells isolated from the IC bladder may represent an increased susceptibility to damage by proinfammatory stimuli.

chronic painful bladder; activated mast cells; neurogenic inflammation

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