The molecular genetic basis of mitochondrial malfunction in bladder tissue following outlet obstruction.
The molecular genetic basis of mitochondrial malfunction in bladder tissue following outlet obstruction.
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DOI：
10.1097/01.ju.0000129560.25005.0e
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发表时间：
2004-08
期刊：
影响因子：
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通讯作者：
R. Levin;A. Hudson
中科院分区：
文献类型：
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作者：
R. Levin;A. Hudson
目的：前列腺增生症常导致膀胱出口部分梗阻后膀胱功能障碍，随着人口老龄化，膀胱功能障碍也越来越常见。最近的研究，从这个和其他群体已经开始阐明的分子基础，充分描述的生理功能障碍，特点是这种临床实体。我们总结和综合了这些信息。材料与方法采用现代分子遗传学方法，包括实时聚合酶链反应、实时逆转录酶-聚合酶链反应等，以及传统的实验技术，如电子显微镜，我们和其他人研究了出口梗阻实验模型中膀胱平滑肌线粒体的转录谱、形态学等。结果许多研究表明，线粒体和线粒体相关核遗传系统的异常基因表达是膀胱出口梗阻后顺应性丧失和其他膀胱功能障碍特征的基础。这种异常的转录特征导致电子传递和氧化磷酸化系统的功能丧失。动物模型系统中线粒体的形态学研究支持这一结论。结论：在很大程度上，出口梗阻后膀胱平滑肌功能的丧失是由于线粒体能量产生的衰减。在这篇文章中，我们回顾和综合了所有可用的实验观察相关的这个问题，我们建议未来的调查线，应该证明富有成效的发展新的战略来治疗的条件。
PURPOSE Bladder dysfunction following partial outlet obstruction is a frequent consequence of benign prostatic hyperplasia and an increasingly common problem given the aging of the general population. Recent studies from this and other groups have begun to elucidate the molecular bases for the well described physiological malfunctions that characterize this clinical entity. We summarized and synthesized that information. MATERIALS AND METHODS Using modern methods of molecular genetics, including real-time polymerase chain reaction, real-time reverse transcriptase-polymerase chain reaction and others, as well as traditional experimental techniques such as electron microscopy we and others examined the transcriptional profile, morphology, etc of bladder smooth muscle mitochondria in experimental models of outlet obstruction. RESULTS Data from many studies have demonstrated that aberrant gene expression in the mitochondrial and mitochondria related nuclear genetic systems underlies the loss of compliance and other attributes of bladder dysfunction following outlet obstruction. Such aberrant transcriptional characteristics engender loss of function in the electron transport and oxidative phosphorylation systems. Morphological studies of mitochondria in the animal model systems support this conclusion. CONCLUSIONS In large part the loss of function in bladder smooth muscle following outlet obstruction results from the attenuation of mitochondrial energy production. In this article we reviewed and synthesized all available experimental observations relevant to this problem and we suggest future lines of inquiry that should prove fruitful in developing new strategies to treat the condition.