학술논문
Estrogen receptor [beta]-deficient female mice develop a bladder phenotype resembling human interstitial cystitis
Document Type
Author abstract
Author
Source
Proceedings of the National Academy of Sciences of the United States. June 5, 2007, Vol. 104 Issue 23, p9806, 4 p.
Subject
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