Decreased abundance of urinary exosomal aquaporin-1 in renal ischemia-reperfusion injury

Decreased abundance of urinary exosomal aquaporin-1 in renal ischemia-reperfusion injury
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DOI:
10.1152/ajprenal.00200.2009
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发表时间:
2009-10-01
影响因子:
4.2
通讯作者:
Ikeda, Masahiro
Ikeda, Masahiro
中科院分区:
医学2区
文献类型:
--
作者:
Sonoda, Hiroko;Yokota-Ikeda, Naoko;Ikeda, Masahiro

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Sonoda H,Yokota-Ikeda N,Oshikawa S,Kanno Y,Yoshinaga K,Uchida K,Ueda Y,Kimiya K,Uezono S,Ueda A,Ito K,Ikeda M在肾缺血再灌注损伤中减少尿液外体水通道蛋白-1的含量。Am J Physiol Renal Physiol 297:F1006-F1016,2009。2009年7月29日首次出版;doi:10.1152/ajprenal。00200.2009.已知从肾上皮细胞分泌到尿液中的尿外切体含有多种类型的肾功能膜蛋白。在此,我们研究了肾缺血再灌注(I/R)对肾I/R大鼠和肾移植患者尿液水通道蛋白-1(AQP1)排泄的影响。免疫印迹分析显示,肾I/R后6h尿液AQP1水平下降,且在I/R后96h仍维持在较低水平。肾脏AQP1的mRNA和蛋白分析表明,尿液AQP1排泄量的减少与早期肾脏AQP1蛋白滞留和晚期肾脏AQP1表达水平降低有关。1例受者在移植后48小时尿液中AQP1的丰度降低。在肾病大鼠模型或蛋白尿患者中,没有观察到尿液外体AQP1的显著下降。我们的研究表明,肾脏AQP1的表达水平可能受其尿液外体排泄的控制,提示尿液外液AQP1是一种新的肾脏I/R损伤的尿液生物标志物。
Sonoda H, Yokota-Ikeda N, Oshikawa S, Kanno Y, Yoshinaga K, Uchida K, Ueda Y, Kimiya K, Uezono S, Ueda A, Ito K, Ikeda M. Decreased abundance of urinary exosomal aquaporin-1 in renal ischemia-reperfusion injury. Am J Physiol Renal Physiol 297: F1006-F1016, 2009. First published July 29, 2009; doi: 10.1152/ajprenal. 00200.2009.-Urinary exosomes, secreted into urine from renal epithelial cells, are known to contain many types of renal functional membrane proteins. Here, we studied whether renal ischemia-reperfusion (I/R) affects urinary exosomal aquaporin-1 (AQP1) excretion in rats subjected to renal I/R and patients who underwent renal transplantation. Immunoblotting studies demonstrated reduction of the urinary exosomal AQP1 level even at 6 h after renal I/R, and the level continued to be low over 96 h after I/R. Renal AQP1 mRNA and protein analyses revealed that the decreased excretion of urinary exosomal AQP1 is associated with renal AQP1 protein retention in the early phase and with a decreased expression level of renal AQP1 in the later phase of renal I/R injury. Decreased abundance of urinary exosomal AQP1 in a recipient patient was also observed at 48 h after renal allograft transplantation. No significant decrease in urinary exosomal AQP1 was observed in a rat model of nephropathy or in patients with proteinuria. Our studies suggest that the renal AQP1 expression level is possibly controlled by its urinary exosomal excretion and indicate that urinary exosomal AQP1 is a novel urinary biomarker for renal I/R injury.