Cheng Cailian, Zheng Zhenda, Shi Chenggang, Liu Xun, Ye Zengchun, Lou Tanqi
Department of Nephrology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510630, P.R. China.
Exp Ther Med. 2013 Dec;6(6):1494-1498. doi: 10.3892/etm.2013.1312. Epub 2013 Sep 23.
The aim of this study was to investigate the effects of advanced glycation end-products (AGEs) on podocyte adhesion and the underlying mechanisms. Immortalized mouse podocytes were exposed to various conditions and podocyte adhesion was evaluated using a hexosaminidase assay. The expression levels of integrin-linked kinase (ILK) were measured by quantitative polymerase chain reaction (qPCR) and western blotting. Treatment with AGEs resulted in a significant, concentration-dependent reduction in podocyte adhesion (P<0.05) and an incremental rise in ILK expression up to a maximum of 100%. Pretreatment with losartan significantly prevented the upregulation of ILK and attenuated the loss of podocyte adhesion observed in podocytes exposed to AGEs (P<0.05). However, the adhesion of losartan-treated podocytes remained lower than that of the podocytes exposed to bovine serum albumin. The results indicate that AGEs reduce podocyte adhesion via the upregulation of ILK expression, which occurs partly through activation of the renin-angiotensin system in podocytes.
本研究的目的是探讨晚期糖基化终产物（AGEs）对足细胞黏附的影响及其潜在机制。将永生化小鼠足细胞置于不同条件下，采用己糖胺酶法评估足细胞黏附情况。通过定量聚合酶链反应（qPCR）和蛋白质印迹法检测整合素连接激酶（ILK）的表达水平。用AGEs处理导致足细胞黏附显著降低，且呈浓度依赖性（P<0.05），ILK表达逐渐升高，最高可达100%。用氯沙坦预处理可显著阻止ILK的上调，并减轻在暴露于AGEs的足细胞中观察到的足细胞黏附丧失（P<0.05）。然而，氯沙坦处理的足细胞的黏附仍低于暴露于牛血清白蛋白的足细胞。结果表明，AGEs通过上调ILK表达降低足细胞黏附，这部分是通过激活足细胞中的肾素-血管紧张素系统实现的。
