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

Prerna Rastogi, Alice Rickard, Nikolay Dorokhov, David J. Klumpp, Jane McHowat*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

15 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)F1129-F1135
JournalAmerican Journal of Physiology - Renal Physiology
Issue number5
StatePublished - May 2008


  • Activated mast cells
  • Chronic painful bladder
  • Neurogenic inflammation

ASJC Scopus subject areas

  • Physiology
  • Urology


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