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Impaired prostaglandin E 2 (PGE 2 ) production in urothelial cells from an interstitial cystitis patient
Author(s) -
Rastogi Prerna,
Dorokhov Nikolay,
Rickard Alice,
McHowat Jane
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.942.7
Subject(s) - interstitial cystitis , prostaglandin e , endocrinology , prostaglandin e2 , tryptase , medicine , chemistry , prostaglandin , stimulation , prostaglandin d2 , cyclooxygenase , urinary system , arachidonic acid , mast cell , immunology , enzyme , biochemistry
SR22 cells are from the inflamed area of the bladder of a patient with interstitial cystitis (IC), a disease characterized by increased activated mast cells in the bladder wall and compromised urothelial function. Since the urinary content of tryptase is increased in IC, this study determined whether there was impairment of prostaglandin E 2 (PGE 2 ) release from SR22 cells in response to tryptase. Responses in SR22 cells were compared to responses observed in PD07i cells derived from a healthy bladder. Interestingly, although PAR‐2 density was significantly lower in SR22 cells, tryptase stimulation of either SR22 or PD07i resulted in a similar increase in phospholipase A 2 activity and arachidonic acid release. However, SR22 cells did not show any increase in PGE 2 release in response to tryptase, whereas there was a significant increase in PGE 2 release from tryptase‐stimulated PD07i. The levels of COX‐1 and COX‐2 mRNA expression were equivalent, but mRNA expression of PGE synthase was considerably lower and of hydroxyprostaglandin dehydrogenase was considerably higher in SR22 compared to PD07i, suggesting that both decreased production and increased metabolism could responsible for the lack of PGE 2 response. Since PGE 2 is cytoprotective, these data may explain why IC is associated with impaired ability to resist cell damage and warrants further investigation. Supported by DK66119 (JM)