Seung Hee Song

Distribution of interstitial cells of cajal and expression of nitric oxide synthase after experimental bladder outlet obstruction in a rat model of bladder overactivity

Recent studies have showed that interstitial cells (ICs) are widely distributed in the genitourinary tract and have suggested their involvement in spontaneous electrical activity and muscle contraction. Nitric oxide (NO) is thought to play a role in bladder overactivity related with bladder outlet obstruction (BOO). The purposes of this study were to investigate the effect of bladder overactivity induced by BOO on ICs and nitric oxide synthase (NOS) isoforms in rat urinary bladder.

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

BACKGROUND Aquaporins (AQPs) have recently been reported to be expressed in rat and human urothelium. Nitric oxide (NO) is thought to play a role in the bladder overactivity related to bladder outlet obstruction (BOO). The purpose of this study is to investigate the effect of BOO on the expression of AQP2-3 and nitric oxide synthase (NOS) isoforms in rat urothelium. METHODS Female Sprague-Dawley rats (230-240 g, n = 60) were divided into 2 groups. The control group (n = 30) and the partial bladder outlet obstruction (BOO) group (n = 30). After 4 weeks, we performed a urodynamic study to measure the contraction interval and contraction pressure. The expression and cellular localization of AQP2-3, endothelial nitric oxide synthase (eNOS) and neuronal nitric oxide synthase (nNOS) were determined by Western blot and immunohistochemistry. RESULTS On the cystometrogram, the estimated contraction interval time (minutes, mean ± SE) was significantly lower in the BOO group (3.0 ± 0.9) than in the control group (6.3 ± 0.4; p < 0.05). AQP2 was localized in the cytoplasm of the epithelium, whereas AQP3 was found only in the cell membrane of the epithelium. The protein expression of AQP2-3, eNOS and nNOS was significantly increased in the BOO group. CONCLUSION Detrusor overactivity induced by BOO causes a significant increase in the expression of AQP2-3, eNOS, and nNOS in rat urinary bladder. This may imply that the AQPs and NOS isoforms have a functional role in the bladder dysfunction that occurs in association with BOO.

An Epidemic of Chronic Pseudophakic Endophthalmitis Due to Ochrobactrum anthropi: Clinical Findings and Managements of Nine Consecutive Cases

Purpose: To report an epidemic of O. anthropi pseudophakic endophthalmitis. Methods: The medical records of nine patients with culture-proven O. anthropi endophthalmitis were reviewed. Results: The presenting features were compatible to chronic endophthalmitis. Two patients showed coinfections with P. acnes. Antibiotics sensitivity test revealed susceptibility to quinolones. Pars plana vitrectomy (PPV) with partial capsulectomy (PC) cured infections in seven patients without coinfection of P. acnes. Final visual acuity was 20/40 or better in five patients. Conclusions: O. anthropi should be considered in cases with chronic pseudophakic endophthalmitis. PPV with PC should be the initial therapeutic option for O. anthropi endophthalmitis.

Expression and Localization of Aquaporins in Benign Prostate Hyperplasia and Prostate Cancer

The aquaporin (AQP) families of water channels are intrinsic membrane proteins that facilitate selective water and small solute movement across the plasma membrane. The purposes of this study were to determine the expression and localization of AQPs in benign prostatic hyperplasia and prostate cancer. Prostatic tissue was collected from patients with benign prostatic hyperplasia or prostate cancer by transurethral resection of the prostate. The expression and cellular localization of the AQPs were determined in the human prostate by Western blot and immunohistochemistry. AQP1, 3, and 9 were expressed in the human prostate. Western blot analysis revealed bands at 28-36 kDa for the AQP1, 3, and 9 proteins. Of these proteins, AQP3 and 9 were expressed in the epithelium. Immunolabeling showed that AQP1 was mainly expressed in the capillaries and venules of the prostate, AQP9 was expressed in the cytoplasm of the epithelium, and AQP3 was mainly associated with the plasma membrane of the prostatic epithelium. Only AQP3 expression was localized in the cell membrane, and expressed AQP3 was translocated to the cytoplasm in prostate cancer. The epithelium in the human prostate expresses AQP3 and 9 proteins, and the capillaries and venules of the prostate express AQP1. Characterizing or modifying the expression of AQP3 may lead to an understanding of the role of the AQPs in human prostatic disease.

Changes in aquaporin 1 expression in rat urinary bladder after partial bladder outlet obstruction: preliminary report.

Purpose 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. Materials and Methods 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. Results 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. Conclusions 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.

Effects of estrogens on the expression of caveolin-1 in the urinary bladders of female rats.

Purpose The purposes of this study were to investigate the effect of hormonal alterations on the expression of caveolin-1 in the urinary bladders of ovariectomized rats and to determine the role of caveolin-1 in the overactivity of the detrusor muscle that occurs with hormonal alterations in rats. Methods Female Sprague-Dawley rats were divided into three groups: a control group, a group that underwent bilateral ovariectomy (Ovx), and a group that underwent bilateral ovariectomy followed by subcutaneous injections of 17β-estradiol (Ovx+Est). After 4 weeks, urodynamic studies were done to measure the contraction interval and contraction pressure. The expression and cellular localization of caveolin-1 were determined by Western blot and immunofluorescence in the urinary bladders of rats. Results On cystometrograms, the contraction interval was significantly shorter in the Ovx group (3.0±0.3 minute) than in the control group (5.6±0.5 minute) but was longer in the Ovx+Est group (9.2±0.4 minute) (P<0.05). Conversely, the average contraction pressure was higher in the Ovx group (26.4±0.48 mmHg) than in the control group (21.8±0.37 mmHg) but was lower in the Ovx+Est group (23.9±0.76 mmHg) (P<0.05). Caveolin-1 was expressed in the capillaries, arterioles, and venules. Expression of the protein caveolin-1 was significantly lower after ovariectomy and was restored to control levels after treatment with 17β-estradiol (P<0.05). Conclusions Hormonal alterations cause a significant change in the expression of caveolin-1, which suggests that caveolin-1 might have a functional role in the overactivity of the detrusor muscle related to hormonal alterations in the urinary bladders of rats.

Early expressions of hypoxia-inducible factor 1alpha and vascular endothelial growth factor increase the neuronal plasticity of activated endogenous neural stem cells after focal cerebral ischemia.

Endogenous neural stem cells become “activated” after neuronal injury, but the activation sequence and fate of endogenous neural stem cells in focal cerebral ischemia model are little known. We evaluated the relationships between neural stem cells and hypoxia-inducible factor-1α and vascular endothelial growth factor expression in a photothromobotic rat stroke model using immunohistochemistry and western blot analysis. We also evaluated the chronological changes of neural stem cells by 5-bromo-2′-deoxyuridine (BrdU) incorporation. Hypoxia-inducible factor-1α expression was initially increased from 1 hour after ischemic injury, followed by vascular endothelial growth factor expression. Hypoxia-inducible factor-1α immunoreactivity was detected in the ipsilateral cortical neurons of the infarct core and peri-infarct area. Vascular endothelial growth factor immunoreactivity was detected in bilateral cortex, but ipsilateral cortex staining intensity and numbers were greater than the contralateral cortex. Vascular endothelial growth factor immunoreactive cells were easily found along the peri-infarct area 12 hours after focal cerebral ischemia. The expression of nestin increased throughout the microvasculature in the ischemic core and the peri-infarct area in all experimental rats after 24 hours of ischemic injury. Nestin immunoreactivity increased in the subventricular zone during 12 hours to 3 days, and prominently increased in the ipsilateral cortex between 3–7 days. Nestin-labeled cells showed dual differentiation with microvessels near the infarct core and reactive astrocytes in the peri-infarct area. BrdU-labeled cells were increased gradually from day 1 in the ipsilateral subventricular zone and cortex, and numerous BrdU-labeled cells were observed in the peri-infarct area and non-lesioned cortex at 3 days. BrdU-labeled cells rather than neurons, were mainly co-labeled with nestin and GFAP. Early expressions of hypoxia-inducible factor-1α and vascular endothelial growth factor after ischemia made up the microenvironment to increase the neuronal plasticity of activated endogenous neural stem cells. Moreover, neural precursor cells after large-scale cortical injury could be recruited from the cortex nearby infarct core and subventricular zone.

Overexpression of aquaporin-1 and caveolin-1 in the rat urinary bladder urothelium following bladder outlet obstruction.

Purpose 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. Methods 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. Results 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). Conclusions 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.

Expression of Caveolin-1 in Rat Urinary Bladder with Cyclophosphamide-Induced Cystitis

Purpose The purposes of this study were to investigate the effect of cyclophosphamide (CYP)-induced inflammatory cystitis on caveolin 1 in rat urinary bladder and to determine the role of these molecules in the bladder dysfunction that occurs in inflammatory change in rat urinary bladder. Methods Female Sprague-Dawley rats were divided into control (n=30) and experimental (n=30) groups. Cystitis in experimental group was induced by intraperitoneal injection of CYP (200 mg/kg). The control group underwent an intraperitoneal saline injection. After 3 days, urodynamic studies were done to measure the contraction interval and contraction pressure. The expression and cellular localization of caveolin 1 were determined by Western blot and immunofluorescent study in rat urinary bladder. Results In cystometrograms, the contraction interval (minute) was significantly increased in the CYP-induced cystitis rats (15.8±1.5) than in the control group (6.3±0.5) (P<0.05). Conversely, the average contraction pressure (mmHg) was significantly higher in the CYP-induced cystitis rats (15.6±1.7) than in the control group (11.3±0.5) (P<0.05). Caveolin 1 was expressed in the capillaries, arteriols and venules. The protein expression of caveolin 1 was significantly decreased in the CYP-induced cystitis rats (P<0.05). Conclusions Inflammatory change of urinary bladder maybe causes a significant change in the expression of caveolin 1. These findings suggest that caveolin 1 might have a functional role in the bladder dysfunction related with cystitis in rat urinary bladder.

Loss of Caveolin 1 is Associated With the Expression of Aquaporin 1 and Bladder Dysfunction in Mice

Purpose: It is suggested that caveolin and aquaporin might be closely associated with bladder signal activity. We investigated the effect of the deletion of caveolin 1, using caveolin 1 knockout mice, on the expression of aquaporin 1 in order to identify their relation in the urothelium of the urinary bladder. Methods: The cellular localization and expressions of aquaporin 1 and caveolin 1, in the wild type and caveolin 1 knockout mice urinary bladder, were examined by Western blot and immunofluorescence techniques. Results: Aquaporin 1 and caveolin 1 were coexpressed in the arterioles, venules, and capillaries of the suburothelial layer in the wild type controls. Aquaporin 1 protein expression was significantly higher in the caveolin 1 knockout mice than in the wild type controls (P <0.05). Conclusions: The results imply that aquaporin 1 and caveolin 1 may share a distinct relation with the bladder signal activity. This might play a specific role in bladder dysfunction.