Article

Changes in Aquaporin 1 Expression in Rat Urinary Bladder after Partial Bladder Outlet Obstruction: Preliminary Report

Department of Urology, Sexual Medical Research Center, Chonnam National University Medical School, Gwangju, Korea.
Korean journal of urology 04/2010; 51(4):281-6. DOI: 10.4111/kju.2010.51.4.281
Source: PubMed

ABSTRACT

Aquaporins (AQPs) are membrane proteins that facilitate water movement across biological membranes. AQPs are also called water channels, and they have recently been reported to be expressed in rat and human urothelium. The purposes of this study were to investigate the effect of bladder outlet obstruction (BOO) on the rat urothelium and AQP1 expression in rat urothelium.
Female Sprague-Dawley rats (230-240 g each, n=20) were divided into 2 groups: the sham group (the Con group, n=10) and the partial BOO group (the BOO group, n=10). The BOO group underwent a partial BOO. The expression and cellular localization of AQP1 were determined by performing Western blotting and immunohistochemistry on the rat urinary bladder.
AQP1 immunoreactivity in both the control and the BOO groups was localized in the capillaries, arterioles, and venules of the lamina propria of the urinary bladder. The protein expression of AQP1 was significantly increased in the BOO group.
This study showed that BOO causes a significant increase in the expression of AQP1. This may imply that AQP1 has a functional role in the detrusor instability that occurs in association with BOO.

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Available from: Kwangsung Park, Dec 20, 2014
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    • "The potential role of aquaporins (AQPs) in the functional alteration of the urinary bladder has been investigated [5-7]. AQPs are a family of transmembrane proteins that mediate water transport across cell membranes [8]. "
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    ABSTRACT: This study was designed to investigate the effect of detrusor overactivity induced by partial bladder outlet obstruction (BOO) on the expression of aquaporin 1 (AQP1) and caveolin 1 (CAV1) in the rat urinary bladder, and to determine the role of these molecules in detrusor overactivity. Female Sprague-Dawley rats were divided into control (n=30) and experimental (n=30) groups. The BOO group underwent partial BOO, and the control group underwent a sham operation. After 4 weeks, an urodynamic study was performed to measure the contraction interval and contraction pressure. The expression and cellular localization of AQP1 and CAV1 were determined by western blot and immunofluorescence experiments in the rat urinary bladder. In cystometrograms, the contraction interval was significantly lower in the BOO group (2.9±1.5 minutes) than in the control group (6.7±1.0 minutes) (P<0.05). Conversely, the average contraction pressure was significantly higher in the BOO group (21.2±3.3 mmHg) than in the control group (13.0±2.5 mmHg) (P<0.05). AQP1 and CAV1 were coexpressed in the capillaries, arterioles, and venules of the suburothelial layer. AQP1 and CAV1 protein expression was significantly increased in the BOO rats compared to the control rats (P<0.05). Detrusor overactivity induced by BOO causes a significant increase in the expression of AQP1 and CAV1, which were coexpressed in the suburothelial microvasculature. This finding suggests that AQP1 and CAV1 might be closely related to bladder signal activity and may have a functional role in BOO-associated detrusor overactivity.
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    • "Animal studies have revealed bladder wall hypertrophy and increased bladder weight after partial BOO [16-18]. Histological analysis has shown smooth muscle cell hypertrophy and hyperplasia and increased collagen deposition, ratio of type I to III collagen, and muscarinic cholinergic receptors [17]. Bladder smooth muscle cell hypertrophy shows widely separated muscle cells with reduction of intermediate cell junctions and collagen deposition in the markedly widened spaces between individual muscle cells and abundant profiles characteristic of enlarged, hypertrophic muscle cells. "
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    ABSTRACT: Bladder wall thickness (BWT) is reported to be related to detrusor overactivity and bladder outlet obstruction. We investigated the relationship between BWT and the responsiveness of storage symptoms to alpha-blockers in men with lower urinary tract symptoms (LUTS). A total of 74 patients with LUTS were enrolled. International Prostate Symptom Score, uroflowmetry with post-void residual urine volume, and transrectal ultrasonography (TRUS) were investigated. BWT was measured by performing TRUS at the midsagittal plane view, and the average value of BWT at the anterior, dome, and trigone areas was used. After 4 weeks of alpha-blocker medication, patients were reevaluated and divided into two groups. The responder group consisted of patients who reported improvement in the storage symptom subscore of 2 points or more; the non-responder group consisted of patients who reported improvement of less than 2 points. Clinical parameters including BWT were compared between the two groups. A total of 52 patients were followed. BWT was positively correlated with intravesical prostate protrusion (IPP) (9.26±4.99, standardized beta=0.393, p=0.002) and storage symptom subscore (0.35±0.43, standardized beta=0.458, p=0.002). Compared with that in the responder group, BWT was thicker in the non-responder group, and improvement in the storage symptom score was correlated with BWT (0.58±0.09 cm vs. 0.65±0.11 cm, p=0.018) and prostate volume (27.08±16.26 ml vs. 36.44±10.1 ml, p=0.018). BWT was correlated with IPP, the storage symptom subscore, and the responsiveness of storage symptoms to alpha-blockers in LUTS/benign prostatic hyperplasia (BPH) patients. As BWT increased, the responsiveness of storage symptoms to alpha-blocker decreased in LUTS/BPH patients.
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    ABSTRACT: The expression of Nitric oxide Synthase (NOS) and aquaporin (AQP) water channels in rat bladder is recently reported. The aim of this study is to evaluate the expression of inducible NOS (iNOS), aquaporin-3 (AQP-3) in cyclophosphamide (CYP) induced rat bladder. The 32 Sprague-Dawley rats were divided into cystitis group (n=20) and control group (n=12). In cystitis group, 100mg/kg CYP was injected every second day for 1 week whereas in control group, normal saline was injected. After extracting of the bladder and dividing dome, body and trigone of the bladder, independently H&E staining and immunohistochemical staining for iNOS and AQP-3 were performed. Expressions of iNOS and AQP-3 were analyzed with a confocal laser scanning microscope and an image analyzer. The expression of iNOS significantly increased in the mucosa, submucosa layer of dome in cystitis group (p<0.05). The expression of AQP-3 significantly increased in the mucosa, submucosa, vessel layer of dome in cystitis group (p<0.05). These results suggest that inflammatory change activates NOS and AQP-3 expression in the bladder tissue of rats. These may imply that NOS and AQP-3 have a pathophyiological role in the cyclophophamide induced interstitial cystitis. Further study on the NOS and AQP-3 in bladder is needed for clinical application.
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