• An-Hsun Chou, Chiou-Mei Lee, Chun-Yu Chen, Jiin-Tarng Liou, Fu-Chao Liu, Ying-Ling Chen, and Yuan-Ji Day.
• Department of Anesthesiology, Chang Gung Memorial Hospital, Linkou, Taipei, Taiwan, ROC; Transgenic & Molecular Immunogenetics Laboratory, Chang Gung Memorial Hospital, Linkou, Taipei, Taiwan, ROC; Department of Medicine, Chang Gung University, Linkou, Taipei, Taiwan, ROC.
• Brain Res. 2014 Sep 25; 1582: 197-210.

AbstractNeurological complications contribute largely to the morbidity and mortality in patients with acute renal failure. In order to study pathophysiological complications of renal failure, a murine model of renal ischemia/reperfusion-induced acute kidney injury (AKI) was generated by 60min bilateral ischemia, and followed by 2h or 24h reperfusion (B-60'IRI). Compared to the sham-operated mice, B-60'IRI mice exhibited a significant inflammatory injury to remote brain. We found that serum and brain levels of KC, G-CSF and MCP-1 were significantly increased in B-60'IRI mice after 2h and 24h reperfusion when compared with sham-operated mice. Moreover, B-60'IRI mice exhibited increased numbers of activated microglial cells in the brain, and severe blood-brain barrier (BBB) permeability when compared with the control sham mice. The technology of cDNA microarray and quantitated RT-PCR are used to identify hippocampal genes whose expression is altered in response to AKI in B-60' IRI mice. The initiation of transcriptional abnormality was indicated by the finding that B-60' IRI mice exhibited upregulated mRNA levels of genes involved in inflammation, cell signaling, extracellular matrix and cell-cycle regulation and downregulated mRNA levels of genes involved in transporters, G protein-coupled receptor signaling, cell survival and chaperone. Our data suggest that renal IR contributes to a complicated hippocampal gene irregulation in inflammation and physiological homeostasis. Copyright © 2014 Elsevier B.V. All rights reserved.

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