Study of the mechanism of tubuloglomerular feedback in macula densa

致密黄斑管球反馈机制研究

• 批准号: 12671053
• 负责人: HASEGAWA Hajime
• 金额: $ 1.73万
• 依托单位: Saitama Medical School (2002)Jikei University School of Medicine (2000-2001)
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2000
• 资助国家: 日本
• 起止时间: 2000 至 2002
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-12671053/
• 关键词: tubuloglomerular feedback; Na-K-2Cl cotransporter; aquaporin; renal failure; DM nephropathy; Na-Cl共輸送体; tubuloglomerular feedback; マクラデンサ; tubulo-glomerular feedback

In this study, the involvement of tubuloglomerular feedback (TGF) abnormality was studied. First, macula densa specific NKCC homolog was identified based on homology cloning strategy. Second, its expression was principally studied by in situ PCR hybridization method. Subsequently, the changes of its gene expression in urinary tract obstruction (UTO) model and non-insulin dependent diabetes mellitus model (NIDDM) were studied. As a results, expression of new clone was decreased in NIDDM, suggesting that its abolished expression might generate the suppression of TGF and expose high pressure to glomerulus, causing glomerulosclerosis.

在这项研究中，肾小管肾小球反馈（TGF）异常的参与进行了研究。首先，基于同源克隆策略鉴定致密斑特异性NKCC同源物。其次，主要采用原位PCR杂交方法研究其表达。随后研究其在尿路梗阻（UTO）模型和非胰岛素依赖型糖尿病（NIDDM）模型中基因表达的变化。结果显示，新克隆在NIDDM中表达减少，表明其表达消失可能会产生TGF的抑制，并使肾小球承受高压，导致肾小球硬化。