EXPRESSION OF CD44 AND E-CADHERIN CELL ADHESION MOLECULES IN HYPERTROPHIED BLADDERS DURING CHRONIC PARTIAL URETHRAL OBSTRUCTION AND AFTER RELEASE OF PARTIAL OBSTRUCTION IN RATS HAYRETTIN OZTURK, HULYA OZTURK, ENSARI GUNELI, YUSUF YAGMUR, AND HUSEYIN BUYUKBAYRAM ABSTRACT Objectives. To determine the functional changes in the bladder and the expression of adhesion molecules in bladder tissue during chronic partial urethral obstruction and after release of partial obstruction in rats. Methods. Twenty-one male Sprague-Dawley rats were separated into three groups, each containing 7 rats. A sham operation was performed in group 1 and cystometry was done 6 weeks later. In groups 2 and 3, hypertrophied unstable bladders were developed by partial infravesical outflow obstruction during a 6-week period. After this period, cystometry was performed in all group 2 rats. In group 3, the ligature was removed, the rats were followed up for 6 weeks, and then cystometry was performed. After cystometric evaluation, the bladders in all the rats were removed, weighed, and studied immunohistopathologically. Results. After release of infravesical outflow obstruction, the bladder weight, residual volume, bladder capacity, maximal voiding pressure, voiding amplitude, and bladder contraction time decreased and bladder compliance increased in group 3 compared with group 2. CD44 and E-cadherin expression in the interstitial space and uroepithelial bladder tissue in group 2 rats stained intensely compared with those of groups 1 and 3. Conclusions. After release of 6 weeks of infravesical outflow obstruction, the cystometric parameters were significantly improved. Expression of CD44 and E-cadherin in the obstructed bladder tissue may be a pathologic sign of inflammation. UROLOGY 65: 1013–1018, 2005. © 2005 Elsevier Inc. I n response to partial urethral obstruction, the bladder smooth muscle hypertrophies to pro- duce the elevated pressures necessary to maintain effective emptying. If the obstruction is left un- treated, the bladder becomes dysfunctional, lead- ing to a significant loss in contractile ability and an increase in the postvoid residual urine volume. 1 It is believed that the etiology for bladder dysfunc- tion secondary to partial outlet obstruction is di- rectly related to neuronal, mitochondrial, and sar- coplasmic reticulum damage. 2 However, the regulatory mechanisms on a molecular and cellular level that mediate the pathogenesis of the detrusor muscle dysfunction are not yet clear. Cell-cell and cell-matrix interactions are among the most basic requirements for many basic func- tions, including differentiation and development of multicellular organisms. These functions are mediated by cell-surface proteins and adhesion molecules. 3 Previous studies noted that adhesion molecules play an important role in organogenesis, healing, inflammation, and progression of malig- nant tumors. 4 Understanding the cellular and mo- lecular mechanisms that determine whether in- flammation resolves or progresses to scarring and tissue destruction should lead to the development of effective therapeutic strategies for inflammatory diseases. 5 The molecular mechanism behind this effect and its potential significance in vivo is a cur- rent focus of research. CD44 and E-cadherin adhe- sion molecules coordinate in targeting leukocytes to sites of infection and inflammation and play an From the Departments of General Surgery, Pediatric Surgery, and Pathology, Dicle University Medical School, Diyarbakır, Turkey; Experimental Animal Research Laboratory, Dokuz Eylul University Medical School, Izmır, Turkey; and Department of Pediatric Surgery, Diyarbakır Children Hospital, Diyarbakır, Turkey Reprint requests: Hayrettin Ozturk, M.D., Department of Pe- diatric Surgery, Dicle University Medical School, Diyarbakır 21280, Turkey. E-mail: ozturkhayrettin@hotmail.com Submitted: July 14, 2004, accepted (with revisions): December 1, 2004 BASIC SCIENCE © 2005 ELSEVIER INC. 0090-4295/05/$30.00 ALL RIGHTS RESERVED doi:10.1016/j.urology.2004.12.006 1013