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Researchers Link IC/BPS Tissue Impairment to Expression of Prostaglandin E2
Marentette JO, Hurst RE, McHowat J. Impaired Expression of Prostaglandin E2 (PGE2) Synthesis and Degradation Enzymes during Differentiation of Immortalized Urothelial Cells from Patients with Interstitial Cystitis/Painful Bladder Syndrome. PLoS One. 2015 Jun 9;10(6):e0129466. doi: 10.1371/journal.pone.0129466. eCollection 2015.
Prostaglandin E2 (PGE2) is naturally occurring, and is probably best known for its role in labor, where it softens the cervix and induces contractions of the uterus. Researchers are making connections between expression of PGE2 and the effects of IC/BPS in the bladder. Recently, Marentette and colleagues looked at cells of the urothelium (i.e. cells lining the urinary tract) taken from patients with IC/BPS. They found that certain substances necessary for development of PGE2 were present in low amounts, and in some cases missing. This helps shed some light on an earlier study from the same group, which showed that urothelial cells taken from patients with IC/BPS weren’t releasing PGE2 as expected when exposed to a specific enzyme that should have provoked its release. Taken together, these findings suggest that in IC/BPS patients, a lack of prostaglandin E2 being released is somehow limiting the normal protective function of urothelial cells, and limiting repair functions when inflammation causes damage to those cells.