Study of the mechanism of tubuloglomerular feedback in macula densa

本研究探讨了TGF异常与肾小管肾小球反馈的关系。首先，基于同源克隆策略，鉴定了黄斑致密特异性NKCC同源基因；其次，主要采用原位PCR杂交法研究其表达。随后，研究其基因在尿路梗阻（UTO）模型和非胰岛素依赖型糖尿病（NIDDM）模型中的表达变化。因此，NIDDM中new clone的表达降低，提示其表达减少可能产生TGF抑制，使肾小球暴露于高压，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.