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The elucidation of crystal formation mechanism through the renal tubular epithelial cell injury and mitochondria injury

通过肾小管上皮细胞损伤和线粒体损伤阐明晶体形成机制

基本信息

批准号：
23791770
负责人：
HIROSE Masahito
金额：
$ 2.66万
依托单位：
Nagoya City University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Young Scientists (B)
财政年份：
2011
资助国家：
日本
起止时间：
2011 至 2012
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23791770/
关键词：
尿路結石女性ホルモン酸化ストレス細胞障害ミトコンドリア

项目摘要

In this study, to elucidate about crystal formation mechanism and the low stone prevalence of the woman, I examined sex differences of crystal formation from oxidative stress and cell injury. Besides, it was aimed for development of new stone prevention by elucidating a relation with a cell injury and the oxidation stress. In the study in 2011, I studied sex differences judging from a renal tubule cell and a mitochondrial injury. I gave an oxalic acid precursor to male and female mice, and clarified a difference of the sex about a renal tubule cell and a mitochondrial injury. In stone model mouse, after oxalic acid precursor administration, mitochondria and microvilli of the renal tubular cell collapsed, aggregated in the renal tubular lumen, and crystal nuclei appeared. With the female mouse, these form changes passed slightly late in comparison with a male. In 2012, I examined osteopontin (OPN) which was a stone-related gene. The expression of OPN in the female mouse had less expression than a male before the crystal formation, and expression increasing was slow. Furthermore, a renal tubular microstructure change was slower than wild type after the treatment of the oxalic acid precursor in the examination using knockout mouse, and there were few cell disorders. And there was little quantity of crystal formation. In the female OPN knockout mouse, there was little quantity of crystals more than male. The results of the study clarified the stone formation mechanism and the importance of mitochondrial injury and oxidative stress. Possibility of the new stone prevention through the mitochondria protection was thought. And these were thought one of the new function of the female hormone.

在这项研究中，为了阐明晶体形成机制和女性结石患病率低，我从氧化应激和细胞损伤方面研究了晶体形成的性别差异。此外，其目的在于通过阐明与细胞损伤和氧化应激的关系来开发新的结石预防。在2011年的研究中，我从肾小管细胞和线粒体损伤来研究性别差异。我给雄性和雌性小鼠草酸前体，并澄清了肾小管细胞和线粒体损伤的性别差异。在结石模型小鼠中，草酸前体给药后，肾小管细胞的线粒体和微绒毛塌陷，聚集在肾小管腔内，并出现晶体核。与雄性小鼠相比，雌性小鼠的这些形态变化稍晚。在2012年，我检查了骨桥蛋白（OPN），这是一种与结石相关的基因。成晶前雌鼠骨桥蛋白的表达量低于雄鼠，且表达量增加缓慢。此外，在使用敲除小鼠的检查中，草酸前体处理后的肾小管微观结构变化比野生型慢，并且几乎没有细胞紊乱。晶体形成量很少。在OPN敲除的雌性小鼠中，晶体的数量比雄性小鼠多很少。研究结果阐明了结石形成机制以及线粒体损伤和氧化应激的重要性。认为通过线粒体保护来预防新结石的可能性。这些被认为是女性荷尔蒙的新功能之一。