Abstract
Bladder symptoms can be ameliorated by sex steroids but to our knowledge the mechanism of action is unknown. Previous studies of steroid receptor expression in the bladder did not indicate receptor subtype expression. We report the distribution of estrogen and progesterone receptor isoforms in the female lower urinary tract. Prospectively recruited women undergoing routine urogynecological or gynecological surgery provided cold cup biopsy samples from the bladder dome, trigone, and proximal and distal urethra. The samples were immediately frozen or fixed in formalin. After RNA extraction transcripts for estrogen receptor alpha and beta, and progesterone receptor A and B were noted on reverse transcriptase-polymerase chain reaction using isoform specific primers. The precise cellular localization of receptor proteins and their relative levels were assessed by immunochemistry in formalin fixed tissue sections with isoform specific antibodies. Nine premenopausal and 10 postmenopausal women were recruited into the study. Two postmenopausal women on hormone replacement therapy. Estrogen receptor alpha and beta, and progesterone receptor A and B transcripts were detected in whole bladder extracts. Nuclear estrogen receptor alpha immunoreactivity was present in squamous epithelium but absent from transitional epithelium. Estrogen receptor beta immunoreactivity was expressed in squamous and transitional cell epithelium. Nuclear progesterone receptor expression was present in urethral squamous epithelium only. Progesterone receptor expression was greater in premenopausal women and in postmenopausal women on estrogen. Estrogen receptor alpha and beta genes are transcribed in bladder tissue but only estrogen receptor beta is translated into protein, suggesting that the urothelium responds to endogenous estrogen via estrogen receptor beta. Progesterone receptor expression is confined to urethral squamous epithelium and the major isoform is progesterone receptor A.
Highlights
The female lower urinary tract is partially derived from the urogenital sinus and is dependent upon the gonadal hormones estrogen and progesterone reproductive life
Previous work before the identification of the estrogen receptors (ER) isoform suggested that transitional epithelium was unable to respond to oestrogen[8], mainly because expression of ER could not be demonstrated
The lack of ER immunoreactivity in transitional epithelium of the present report supports some of the previous findings[6]
Summary
The female lower urinary tract is partially derived from the urogenital sinus and is dependent upon the gonadal hormones estrogen and progesterone reproductive life. Bladder capacity, detrusor contractility and flow rates are reduced and estrogen supplementation relieves the symptoms of urinary urgency in postmenopausal women[1]. Estrogen significantly reduces the re-infection rate in post-menopausal women with recurrent urinary tract infections[2]. Estrogen and progesterone action is mediated by high affinity intracellular receptors[3]. Ligand-bound receptors translocate to the nucleus to act as transcription factors regulating gene expression. Recent evidence points to multiple isoforms of estrogen receptors (ER) and progesterone receptors (PR) being generated from each gene. The main ER isoforms studied in other tissues have been ER and ER 4, and the main PR isoforms studied have been PR-A and PR-B5
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