학술논문

Estrogen receptor [beta]-deficient female mice develop a bladder phenotype resembling human interstitial cystitis
Document Type
Author abstract
Source
Proceedings of the National Academy of Sciences of the United States. June 5, 2007, Vol. 104 Issue 23, p9806, 4 p.
Subject
United States
Language
English
ISSN
0027-8424
Abstract
Interstitial cystitis/painful bladder syndrome is a disease seen mostly in women, and symptoms tend to be worse premenopausally or during ovulation. The four cardinal symptoms of interstitial cystitis/painful bladder syndrome are bladder pain, urgency, frequency, and nocturia. Estrogen has been implicated in the etiology of this disease, but the role of the two estrogen receptors (ER), ER[alpha] and ER[beta], has not been investigated. We found that, in the bladders of WT mice, ER[beta] is expressed in the basal cell layer of the urothelium. Bladders of male ER[[beta].sup.-/-] mice were intact and morphologically indistinguishable from those of their WT littermates. However, in female ER[[beta].sup.-/-] mice, there was ulceration and atrophy of bladder urothelium concomitant with infiltration of [[gamma].sup.[delta]] T cells concentrated in the areas of atrophy and shedding of urothelium. The data support the idea that activated T cells are causing the damage to the urothelium. The hyperactivity of T cells may be because of an imbalance between ER[alpha] and ER[beta] signaling in female ER[[beta].sup.-/-] mice. Our data suggest that reduced ER[beta] signaling might have a role in the pathogenesis of interstitial cystitis, and ER[beta] could be a candidate for a target of medical therapy. [[gamma].sup.[delta]] T cells | urothelium | painful bladder syndrome