Decreased Angiopoietin Expression in Underactive Bladder Induced by Long-term Bladder Outlet Obstruction.

IF 1.8 3区 医学 Q3 UROLOGY & NEPHROLOGY
International Neurourology Journal Pub Date : 2023-12-01 Epub Date: 2023-12-31 DOI:10.5213/inj.2346296.148
Jae Heon Kim, Hee Jo Yang, Hong Jun Lee, Yun Seob Song
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引用次数: 0

Abstract

Purpose: Ischemia of the bladder can occur if neovascular formation cannot keep pace with hypoxia induced by chronic bladder outlet obstruction (BOO). The aim of this study was to examine changes in angiogenesis growth factor expression generated by chronic BOO in a rat model of underactive bladder.

Methods: Twenty female Sprague-Dawley rats aged 6 weeks were assigned to 4 groups (5 rats per group). Group 1 was the control. Group 2 underwent sham surgery. The rats in groups 3 and 4 underwent BOO and were followed up for 1 week and 8 weeks. Cystometry was carried out together with bladder tissue analysis at 1 week and 8 weeks postoperatively. Real-time polymerase chain reaction (PCR) assays were conducted to determine the expression level of angiogenesis-related growth factors. A hypoxia signaling pathway PCR array was additionally carried out.

Results: The group that underwent BOO for 8 weeks showed abnormal bladder function, with a diminished intercontraction interval, decreased maximal voiding pressure, and higher volume of residual urine (P<0.05). Hypoxia-inducible factor-1 alpha expression was elevated in this group. The expression levels of vascular endothelial growth factor (VEGF) and VEGF receptor messenger RNA (mRNA) in the BOO group were comparable to those in the control group. However, angiotensin/tie receptor mRNA expression levels increased at 1 week after BOO, but decreased at 8 weeks after BOO. In animals that underwent BOO, fewer blood vessels exhibited positive immunofluorescent staining for von Willebrand factor. Alterations were also seen in the hypoxia signaling pathway PCR array.

Conclusion: In a rat model of underactive bladder caused by surgical BOO, reduced angiopoietin expression was demonstrated. This observation might underlie visceral ischemia and fibrosis associated with the procedure. The findings of this study might offer an improved understanding of the disease processes underlying BOO and facilitate selection of the appropriate time to repair the organ in this condition.

长期膀胱出口梗阻导致膀胱功能减退时血管生成素表达减少
目的:如果新生血管的形成跟不上慢性膀胱出口梗阻(BOO)引起的缺氧,就会导致膀胱缺血。本研究旨在研究慢性膀胱出口梗阻引起的血管生成生长因子表达的变化:将 20 只年龄为 6 周的雌性 Sprague-Dawley 大鼠分为 4 组(每组 5 只)。第 1 组为对照组。第 2 组接受假手术。第 3 组和第 4 组的大鼠接受了 BOO,并分别接受了 1 周和 8 周的随访。在术后 1 周和 8 周进行膀胱测量和膀胱组织分析。进行实时聚合酶链反应(PCR)检测,以确定血管生成相关生长因子的表达水平。此外,还进行了缺氧信号通路 PCR 阵列分析:结果:连续 8 周接受 BOO 治疗的大鼠组显示出膀胱功能异常,收缩间期缩短,最大排尿压降低,残余尿量增加(PC结论:在大鼠膀胱功能减退模型中,血管生成相关生长因子的表达水平与大鼠膀胱功能减退的程度成正比:在一个由手术切除膀胱引起的膀胱功能不全的大鼠模型中,血管生成素的表达减少了。这一观察结果可能是与手术相关的内脏缺血和纤维化的原因。这项研究的结果可能有助于人们更好地了解膀胱癌的发病过程,并有助于在这种情况下选择修复器官的适当时机。
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来源期刊
International Neurourology Journal
International Neurourology Journal UROLOGY & NEPHROLOGY-
CiteScore
4.40
自引率
21.70%
发文量
41
审稿时长
4 weeks
期刊介绍: The International Neurourology Journal (Int Neurourol J, INJ) is a quarterly international journal that publishes high-quality research papers that provide the most significant and promising achievements in the fields of clinical neurourology and fundamental science. Specifically, fundamental science includes the most influential research papers from all fields of science and technology, revolutionizing what physicians and researchers practicing the art of neurourology worldwide know. Thus, we welcome valuable basic research articles to introduce cutting-edge translational research of fundamental sciences to clinical neurourology. In the editorials, urologists will present their perspectives on these articles. The original mission statement of the INJ was published on October 12, 1997. INJ provides authors a fast review of their work and makes a decision in an average of three to four weeks of receiving submissions. If accepted, articles are posted online in fully citable form. Supplementary issues will be published interim to quarterlies, as necessary, to fully allow berth to accept and publish relevant articles.
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