Effects of varying degrees of partial bladder outlet obstruction on urinary bladder function of rats: A novel link to inflammation, oxidative stress and hypoxia

2017 ◽  
Vol 11 (2) ◽  
pp. O193-O201 ◽  
Author(s):  
Ecem Kaya Sezginer ◽  
Didem Yilmaz‐Oral ◽  
Utku Lokman ◽  
Serpil Nebioglu ◽  
Fugen Aktan ◽  
...  
Urology ◽  
2009 ◽  
Vol 73 (6) ◽  
pp. 1417-1422 ◽  
Author(s):  
Fei Liu ◽  
Liping Yao ◽  
Jianlin Yuan ◽  
Heliang Liu ◽  
Xiaojian Yang ◽  
...  

2021 ◽  
Author(s):  
Menjiang Tu ◽  
Rui Wang ◽  
Pei Zhu ◽  
Qingqing Wang ◽  
Bishao Sun ◽  
...  

Abstract Background: Partial bladder outlet obstruction (pBOO), a common urological disease, often results in bladder tissue inflammation and remodeling. Human urine-derived stem cells (USCs) have demonstrated therapeutic benefits in various organ injury models. We used a rat model of pBOO to investigate the effect of USCs on bladder function and to explore the miRNA and gene expression profiles in bladder tissue using RNA sequencing.Methods: In total, 18 rats were randomly and evenly assigned to the following three groups: a sham surgery group, a pBOO without USC therapy group, and a pBOO with USC therapy group (subjected to treatment with USCs six times every other week). All rats were subjected to routine urodynamic monitoring. Detrusor muscle strips were analyzed and pathophysiology was assessed. Finally, altered miRNA and mRNA expression profiles of bladder tissue were examined using RNA sequencing and bioinformatics analysis technology.Results: After USC treatment, urodynamic monitoring revealed elevated bladder compliance and maximal voiding pressure, declined end filling pressure and voided volume, and improved detrusor muscle contractility and carbachol sensitivity in pBOO rats. Histology and TUNEL assay revealed reduced collagen deposition and muscle cell apoptosis in bladder tissue. The differential expression of eight miRNAs in pBOO rats was reversed by USC treatment. Bioinformatics analysis helped identify miR-142 and miR-9a as the two largest nodes of differentially expressed miRNAs in the miRNA‑gene interaction network in the USC-treated group. The Kyoto Encyclopedia of Genes and Genomes analysis revealed enrichment of multiple significant pathways, including those involved in necroptosis and cytokine-cytokine receptor interactions.Conclusions: This is the first study to reveal the protective effect of USCs on bladder function and bladder remodeling in pBOO rats. The miRNA and mRNA expression levels differed in the bladder of pBOO rats with and without USC treatment. Although the mechanism underlying these effects has not been fully elucidated, necroptosis and cytokine-cytokine receptor interaction-related pathways may be involved.


2017 ◽  
Vol 313 (5) ◽  
pp. F1149-F1160 ◽  
Author(s):  
Nao Iguchi ◽  
M. İrfan Dönmez ◽  
Anna P. Malykhina ◽  
Alonso Carrasco ◽  
Duncan T. Wilcox

Posterior urethral valves are the most common cause of partial bladder outlet obstruction (PBOO) in the pediatric population. Pathological changes in the bladder developed during PBOO are responsible for long-lasting voiding dysfunction in this population despite early surgical interventions. Increasing evidence showed PBOO induces an upregulation of hypoxia-inducible factors (HIFs) and their transcriptional target genes, and they play a role in pathophysiological changes in the obstructed bladders. We hypothesized that blocking HIF pathways can prevent PBOO-induced bladder dysfunction. PBOO was surgically created by ligation of the bladder neck in male C57BL/6J mice for 2 wk. PBOO mice received intraperitoneal injection of either saline or 17-DMAG (alvespimycin, 3 mg/kg) every 48 h starting from day 1 postsurgery. Sham-operated animals received injection of saline on the same schedule as PBOO mice and served as controls. The bladders were harvested after 2 wk, and basal activity and evoked contractility of the detrusor smooth muscle (DSM) were evaluated in vitro. Bladder function was assessed in vivo by void spot assay and cystometry in conscious, unrestrained mice. Results indicated the 17-DMAG treatment preserved DSM contractility and partially prevented the development of detrusor over activity in obstructed bladders. In addition, PBOO caused a significant increase in the frequency of micturition, which was significantly reduced by 17-DMAG treatment. The 17-DMAG treatment improved urodynamic parameters, including increases in the bladder pressure at micturition and nonvoid contractions observed in PBOO mice. These results demonstrate that treatment with 17-DMAG, a HIF inhibitor, significantly alleviated PBOO-induced bladder pathology in vivo.


2018 ◽  
Author(s):  
Min Soo Choo ◽  
SongZhe Piao ◽  
Seung-June Oh

AbstractAIMSTo investigate the effect of a free radical scavenger (tempol) after relief of partial bladder outlet obstruction (pBOO) on bladder function in a rat model.METHODSpBOO was induced in 50 eight-week-old female Sprague-Dawley rats and relieved 3 weeks later. The rats were divided randomly into 5 groups: sham-operated, tempol-treated for 1 week (Treat-1w) or 3 weeks (Treat-3w), and no treatment for 1 week (nonTreat-1w) or 3 weeks (nonTreat-3w). Awaken cystometrograms were obtained 1 or 3 weeks after relief according to the grouping. The bladders were isolated and weighed. H&E, Masson’s trichrome and TUNEL staining were used to analyze histological changes. The oxidative stress assessed using malondialdehyde. The expression of beta-3 adrenoreceptor was examined by Western blotting.RESULTSThe tempol-treated groups exhibited a significant decrease in the number of IDCs per voiding cycle (nonTreat-1w vs. Treat-1w, 1.18±0.82 vs. 0.36±0.40, P=0.010; nonTreat-3w vs. Treat-3w, 1.51±0.69 vs. 0.23±0.25, P=0.002). The thickness and collagen fiber deposition of the detrusor muscle layer was significantly decreased in the treated groups. Apoptosis detected was mainly observed in the urothelial cell layer, although the rate of apoptosis was significantly decreased in the treated groups (48.9±3.36% vs. 32.7±11.10%, P=0.024; 25.8±4.67% vs. 15.7±9.83%, P=0.314). The tempol-treated groups showed significant decreases in the MDA concentrations at both 1 and 3 weeks after relief. The expression of the beta-3 adrenoreceptor was increased in the tempol-treated rats.CONCLUSIONSIschemic reperfusion injury after relief of pBOO caused histological and functional changes in the bladder. Free radical scavenger treatment prevented this oxidative stress.


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