The Expression of AQP1 and eNOS in Menopausal Rat Urinary Bladder

Abstract

Purpose: Aquaporins (AQPs) have been reported to be expressed in rat and human urothelium. Nitric oxide (NO) is thought to play an important role in the bladder overactivity related to menopause. The purpose of this study was to investigate the effect of hormonal alteration on the expression of AQP1 and eNOS in menopausal rat urinary bladder. Materials and Methods: Female Sprague-Dawley rats (230-240 g, N=30) were divided into three groups: control (N=10), bilateral ovariectomy (Ovx, N=10), and bilateral ovariectomy followed by subcutaneous injections of 17β -estradiol (50 mg/kg/day, Ovx+Est, N=10). After 4 weeks, urodynamic studies measuring the contraction interval and contraction pressure were done. The expression and cellular localization of AQP1 and eNOS were determined by performing Western blotting and immunohistochemistry on the rat urinary bladder. Results: The approximate contraction interval (min) was significantly decreased in the Ovx group (3.9±0.25) compared to the control group (6.7±0.15), and was increased after estrogen treatment (9.7±0.22) (p<0.05). The AQP1 and eNOS immunoreactivities were localized in the same areas: capillaries, arterioles, and venules of the lamina propria. The protein expression of AQP1 was not changed significantly, whereas eNOS expression was significantly decreased in the Ovx group and restored to the control value in the Ovx+Est group. Conclusions: This study showed that ovariectomy causes a significant change in e-NOS expression without a change in AQP1 in menopausal rat urinary bladder. This may imply that e-NOS has a functional role in the bladder overactivity that occurs in association with menopause.

Effect of detrusor overactivity on the expression of aquaporins and nitric oxide synthase in rat urinary bladder following bladder outlet obstruction

“…In our previous study, we reported that AQP1 was mainly expressed in the capillaries and venules of the urinary bladder and that significantly increased protein expression of AQP1 in the BOO rat urinary bladder. 13 In the current study, immunolabeling of AQP2 was expressed throughout the epithelial cell layer and detrusor smooth muscle, and AQP3 was expressed only throughout the epithelial cell layer.…”

“…12 Recently, we reported AQP1 expression in the capillaries and venules of the urinary bladder and significant incease of protein expression of AQP1 in the BOO rat urinary bladder. 13 No studies to date have investigated the expression of AQP2-3 in the urinary bladder of rats after BOO or the functional activity of these proteins in response to BOO.…”

Transplantation of Brain-Derived Neurotrophic Factor-Expressing Mesenchymal Stem Cells Improves Lower Urinary Tract Symptoms in a Rat Model

“…Taken together, our results showed engrafted stem cells to accelerate the rebuilding of bladder tissue by upregulating Ang1 and PDGF expression. High eNOS expression due to the stem cells also improved the restoration of damaged bladder, thereby contributing to functional improvement of the bladder [20][21][22]. We had previously observed the functional efficacy of SDF-1-overexpressing MSCs in an NB rat model [10];…”

Signalling Molecules in the Urothelium

“…Nevertheless, Giglio et al [ 48 ] have shown that 60 hours after a single intraperitoneal injection of cyclophosphamide in rats, at a time point when the innate inflammatory response is at its peak, the expression of eNOS seems to be heavily increased in the urothelium and suburothelium. Several other studies have also revealed that the expression of eNOS can vary greatly during certain disease states [ 113 , 120 ]. Apart from the urothelium, there seems to be several other sources for nitric oxide in the urinary bladder, that is, interstitial cells in the lamina propria [ 48 ] and various nerves [ 121 – 123 ].…”