Study of the mechanism of tubuloglomerular feedback in macula densa

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。结果表明，NIDDM时新克隆表达减少，提示其表达缺失可能产生TGF抑制，使肾小球高压暴露，导致肾小球硬化。

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.