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.