Feng Wei, Tang Rongwei, Ye Xudong, Xue Chao, Liao Yunhua
Department of Nephrology, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Kidney Blood Press Res. 2016;41(1):48-54. doi: 10.1159/000368546. Epub 2016 Feb 4.
BACKGROUND/AIMS: Ischemia-reperfusion (IR) injury in the kidney is a major cause of acute kidney injury in humans. However, the molecular mechanisms responsible for the progression of kidney IR injury still need to be explored. In this study, we aimed to explore the underlying genes and pathways associated with kidney IR injury.
Gene microarray of GSE27274 was downloaded from the Gene Expression Omnibus database. The differentially expressed genes (DEGs) between kidney IR injury and kidney IR rat samples were analyzed. Gene Ontology biological process (BP) and pathway enrichment analyses of DEGs were performed, followed by protein-protein interaction (PPI) network construction.
A total of 88 up-regulated and 102 down-regulated DEGs were identified. The up-regulated DEGs including FK506 binding protein 1A (Fkb1a) were mainly enriched in biological processes (BPs) related to protein ubiquitination. The down-regulated DEGs including complement component 5 (C5) were enriched in complement and coagulation cascades pathway. Choline phosphotransferase 1 (Chpt1) was enriched in glycerophospholipid metabolism pathway. In the PPI network, heme oxygenase (decycling) 1 (Hmox1) was as a hub gene that interacted with the maximum nodes.
DEGs of Fkb1a, C5, Chpt1, and Hmox1, as well as complement and coagulation cascades pathway, glycerophospholipid metabolism pathway, and BP terms related to protein ubiquitinatione may be the potential targets for diagnosis and treatment of kidney IR injury.
背景/目的：肾脏缺血再灌注（IR）损伤是人类急性肾损伤的主要原因。然而，导致肾脏IR损伤进展的分子机制仍有待探索。在本研究中，我们旨在探索与肾脏IR损伤相关的潜在基因和通路。
从基因表达综合数据库下载GSE27274基因芯片。分析肾脏IR损伤和肾脏IR大鼠样本之间的差异表达基因（DEG）。对DEG进行基因本体生物学过程（BP）和通路富集分析，随后构建蛋白质-蛋白质相互作用（PPI）网络。
共鉴定出88个上调和102个下调的DEG。上调的DEG包括FK506结合蛋白1A（Fkb1a），主要富集在与蛋白质泛素化相关的生物学过程（BP）中。下调的DEG包括补体成分5（C5），富集在补体和凝血级联途径中。胆碱磷酸转移酶1（Chpt1）富集在甘油磷脂代谢途径中。在PPI网络中，血红素加氧酶（去环化）1（Hmox1）是与最大节点相互作用的枢纽基因。
Fkb1a、C5、Chpt1和Hmox1的DEG，以及补体和凝血级联途径甘油磷脂代谢途径和与蛋白质泛素化相关的BP术语可能是肾脏IR损伤诊断和治疗的潜在靶点。
