权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Investigation the mechanism of renal stone formation by used the MDCK cell line.

利用MDCK细胞系研究肾结石形成的机制。

基本信息

批准号：
11671547
负责人：
OHTAWARA Yosihisa
金额：
$ 2.37万
依托单位：
Hamamatsu University School of Medicine
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1999
资助国家：
日本
起止时间：
1999 至 2001
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11671547/
关键词：
MDCK cell oxalic acid calculus renal tubular epithelial cells nephrolith phosphoric acid calculus UIT PGE2 vit. K 腎結石シュウ酸結石 UTI 尿路結石ショウ酸結石オステオポンチン

项目摘要

This study elucidates a cause of the calculus formation by making a model of humans nephrolith with a cultured cell. However, I was careless by making of an oxalic acid calculus.Model making of an oxalic acid calculus uses animal experiment together simultaneously, and a thought colander will not get transplant to an animal of MDCK cells. The renal tubular epithelial cells of a different kind animal was used in addition to a MDCK cells by this study, and the difference was examined, but the generation of a phosphoric acid calcium calculus was specifically watched only to a MDCK cell. We think that this participates in specific calcium ion transportation ability of this cell. It was suggested that vit. K and PGE2 participated in accumulation of the calcium for stone formation.As a result of having measured the UIT density in urine from a calculus patient of humans, we thought that it was effective in the UIT for calculus prevention.The osteopontin density known as one of a cause of calculus form was measured during urine of humans calculus patient, and we thought to be a promotion factor of the calculus formation.The calculus ingredient which a MDCK cell generates is different from oxalic acid calcium, and examination of these restraint factors and a promotion factor is not done enough this time because it is phosphoric acid calcium. If it is possible, a model forming an oxalic acid calcium calculus in this cell is done sequentially in future, and it is necessary to make clear it about these factors.

本研究通过培养细胞建立人肾结石模型，阐明了结石形成的原因。然而，我不小心做了一个草酸结石，草酸结石的模型制作同时使用动物实验，而且认为漏勺不会移植到MDCK细胞的动物身上。在本研究中，除了MDCK细胞之外，还使用了不同种类动物的肾小管上皮细胞，并检查了差异，但仅对MDCK细胞具体观察了磷酸钙结石的产生。我们认为这参与了该细胞的特异性钙离子转运能力。有人说，vit。K和PGE 2参与了结石形成的钙的积累。由于测量了人类结石患者尿液中的UIT密度，我们认为UIT对预防结石是有效的。测量了人类结石患者尿液中的骨桥蛋白密度，MDCK细胞产生的结石成分不同于草酸钙，并且由于它是磷酸钙，所以这次对这些抑制因子和促进因子的检查做得不够。如果可能的话，今后将依次建立在该细胞中形成草酸钙结石的模型，有必要明确这些因素。