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Impaired expression of prostaglandin E 2 synthesis and degradation enzymes in urothelial cells from patients with interstitial cystitis.
Author(s) -
McHowat Jane,
Rickard Alice,
Marentette John
Publication year - 2010
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.24.1_supplement.999.4
Subject(s) - urothelium , urothelial cell , interstitial cystitis , prostaglandin , cyclooxygenase , endocrinology , chemistry , medicine , cell culture , prostaglandin e , cellular differentiation , andrology , enzyme , urinary bladder , biology , urinary system , biochemistry , gene , genetics
The differentiated superficial cells of the urothelium restrict urine flow into the bladder wall. We have demonstrated that urothelial cells isolated from bladders of patients with interstitial cystitis (IC) fail to release PGE 2 in response to tryptase. We measured protein expression of 15‐hydroxyprostaglandin dehydrogenase (PGDH), cyclooxygenase‐2 (COX‐2) and prostaglandin E 2 synthase (PGES) in immortalized urothelial cells isolated from the bladders of IC patients (SR22A, SM28) or normal subjects (PD07i, PD08i) during differentiation produced by increased calcium and fetal bovine serum in the culture medium for 1, 3 and 7 days. PGES expression increased during differentiation in normal and IC urothelial cells. COX‐2 expression also increased in cells from normal patients following differentiation. Remarkably, no COX‐2 expression was detectable in IC cells. PGDH decreased in normal cells after 1 and 3 days of differentiation, but returned to normal after 7 days. PGDH expression was unchanged during differentiation at 1 and 3 days, but was more than 2‐fold higher at 7 days compared to day 0 in the IC cells. Urothelial cells isolated from IC patients demonstrated no PGE 2 release in response to tryptase under any of the experimental conditions studied. Taken together, our results indicate that PGE 2 release is compromised during differentiation in IC urothelium and may contribute to impaired barrier function.