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

doi:10.1152/ajprenal.00572.2007

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

Journal article

Open access

Peer reviewed

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

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

American journal of physiology. Renal physiology, Vol.294(5), pp.F1129-1135

05/2008

DOI: 10.1152/ajprenal.00572.2007

PMCID: PMC2830562

PMID: 18322019

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Abstract

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 A(2) (PLA(2)) activity and the resultant release of arachidonic acid and prostaglandin E(2) (PGE(2)). Tryptase stimulation of either PD07i or SR22A resulted in similar increases in PLA(2) activity and arachidonic acid release. However, tryptase stimulation of SR22A and SM28 abn did not result in a significant increase in PGE(2) release compared with the increase in PGE(2) 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 PGE(2) response in tryptase-stimulated SR22A cells. Since PGE(2) 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.

Protein Folding

Intramolecular Oxidoreductases - biosynthesis

Tryptases - metabolism

Arachidonic Acid - metabolism

Urothelium - metabolism

Gene Expression - drug effects

Humans

Group VI Phospholipases A2 - biosynthesis

Cytoprotection - physiology

Urinary Bladder - pathology

Cadherins - biosynthesis

Urothelium - pathology

Cyclooxygenase 2 - biosynthesis

Keratins - biosynthesis

Group VI Phospholipases A2 - genetics

Cystitis, Interstitial - metabolism

Cell Line

Urinary Bladder - metabolism

Hydroxyprostaglandin Dehydrogenases - biosynthesis

Phospholipases A2 - metabolism

Enzyme Activation - drug effects

Dinoprostone - metabolism

Cystitis, Interstitial - pathology

Prostaglandin-E Synthases

Wound Healing - physiology

Details

Title: Subtitle: Loss of prostaglandin E2 release from immortalized urothelial cells obtained from interstitial cystitis patient bladders
Creators: Prerna Rastogi - Department of Pathology, Saint Louis University School of Medicine, Doisy Research Bldg., 3rd Floor, 1110 S. Grand Blvd., St. Louis, MO 63104, USA
Alice Rickard
Nikolay Dorokhov
David J Klumpp
Jane McHowat
Resource Type: Journal article
Publication Details: American journal of physiology. Renal physiology, Vol.294(5), pp.F1129-1135
DOI: 10.1152/ajprenal.00572.2007
PMID: 18322019
PMCID: PMC2830562
NLM abbreviation: Am J Physiol Renal Physiol
ISSN: 1931-857X
eISSN: 1522-1466
Publisher: United States
Grant note: DK-66119 / NIDDK NIH HHS R01 DK066119 / NIDDK NIH HHS R01 DK066119-04 / NIDDK NIH HHS
Language: English
Date published: 05/2008
Academic Unit: Pathology
Record Identifier: 9984047893302771

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