Nod1 and nod2 are expressed in human and murine renal tubular epithelial cells and participate in renal ischemia reperfusion injury.
Nod1 and nod2 are expressed in human and murine renal tubular epithelial cells and participate in renal ischemia reperfusion injury.
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NOD1和NOD2在人和鼠肾小管上皮细胞中表达，并参与肾脏缺血再灌注损伤。
DOI：
10.4049/jimmunol.0903065
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发表时间：
2010-03-01
期刊：
影响因子：
--
通讯作者：
McKay DB
中科院分区：
文献类型：
--
作者：
Shigeoka AA;Kambo A;Mathison JC;King AJ;Hall WF;da Silva Correia J;Ulevitch RJ;McKay DB
Nod1和Nod2是细胞内先天感受器家族的成员，其参与对组织损伤过程中释放的病原体和分子的先天免疫应答，包括由缺血诱导的损伤。肾脏缺血性损伤以肾小管上皮细胞凋亡和炎症为特征。已知对细胞凋亡和炎症有贡献的细胞内先天免疫受体中研究得最好的是Nod1和Nod2。我们的研究比较和对比了野生型小鼠和Nod 1、Nod 2、Nod（1×2）及其下游信号分子Rip2缺陷小鼠的肾缺血效应。我们发现Nod1和Nod2存在于小鼠和人肾上皮细胞的肾小管上皮细胞中，并且这些受体在小鼠中的缺失导致对肾缺血再灌注损伤的保护。在Nod2和Rip2缺乏的情况下观察到对肾损伤的显著保护，并且同时缺乏Nod1和Nod2提供了更大的保护。我们的结论是细胞内传感器Nod1和Nod2在急性缺血性肾损伤的发病机制中起着重要的作用，虽然可能通过不同的机制。
Nod1 and Nod2 are members of a family of intracellular innate sensors that participate in innate immune responses to pathogens and molecules released during the course of tissue injury, including injury induced by ischemia. Ischemic injury to the kidney is characterized by renal tubular epithelial apoptosis and inflammation. Among the best studied intracellular innate immune receptors known to contribute to apoptosis and inflammation are Nod1 and Nod2. Our study compared and contrasted the effects of renal ischemia in wild-type mice and mice deficient in Nod1, Nod2, Nod (1×2) and in their downstream signaling molecule Rip2. We found that Nod1 and Nod2 were present in renal tubular epithelial cells in both mouse and human kidney epithelial cells and that the absence of these receptors in mice resulted in protection from kidney ischemia reperfusion injury. Significant protection from kidney injury was seen with a deficiency of Nod2 and Rip2, and the simultaneous deficiency of Nod1 and Nod2 provided even greater protection. We conclude that the intracellular sensors Nod1 and Nod2 play an important role in the pathogenesis of acute ischemic injury of the kidney, although possibly through different mechanisms.
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影响因子：
19.6
作者：
Awad, Alaa S.;Rouse, Michael;Huang, Liping;Vergis, Amy L.;Reutershan, Joerg;Cathro, Helen P.;Linden, Joel;Okusa, Mark D.
通讯作者：
Okusa, Mark D.
DOI：
10.1159/000142934
发表时间：
2008
期刊：
Nephron. Experimental nephrology
影响因子：
--
作者：
Kinsey GR;Li L;Okusa MD
通讯作者：
Okusa MD
影响因子：
19.6
作者：
Kaushal, GP;Basnakian, AG;Shah, SV
通讯作者：
Shah, SV
影响因子：
15.9
作者：
Leemans, JC;Stokman, G;Florquin, S
通讯作者：
Florquin, S
影响因子：
12.4
作者：
Correia, J. da Silva;Miranda, Y.;Ulevitch, R. J.
通讯作者：
Ulevitch, R. J.