Genome-wide gene expression profiling of ischemia-reperfusion injury in rat kidney, intestine and skeletal muscle implicate a common involvement of MAPK signaling pathway

The mechanisms of ischemia-reperfusion (I/R) injury have not been fully elucidated to date. In order to determine the genetic involvement across different organs during I/R injury, a DNA microarray approach was used to analyze the gene expression profiles of the kidney, intestine, and skeletal muscle in a rat model of I/R injury. Fifteen male Lewis rats were divided randomly into three different organ groups; a sham operation (control group), 60-min-ischemia (Is group) only, and 60-min-ischemia plus 60-min-reperfusion (I/R group), respectively. The target genes were identified by DNA microarray and studied by quantitative polymerase chain reaction (qPCR). By comparing the I/R group with the control group, a 2-fold upregulation of 467, 172, and 3932 and a 2-fold downregulation of 437, 416, and 4203 genes were identified in the kidney, small intestine, and skeletal muscle, respectively. Several commonly upregulated genes associated with mitogen-activated protein kinase (MAPK) pathways, including Jun, Atf3, junB, Fos, Adm and Dusp 1, were differentially expressed in the I/R group. The mRNA expression levels of the target genes were confirmed by qPCR. The present study hypothesized that the MAPK pathway may function in a common pathway of I/R injury and regulate the pathogenesis through activator protein 1. The findings of the present study contributed to the understanding of the molecular pathways associated with I/R injury.