Accumulating evidence indicates that ischemia reperfusion (IR) injury is caused by a burst of reactive oxygen species (ROS) generated during reperfusion.  Neutrophils, cells that contain the machinery for producing O2 radicals, are considered the main culprits of this IR injury. The excessive infiltration of these inflammatory cells with subsequent release of cytotoxic and chemotactic mediators contributes to cellular damage. A recent study has linked a transcription factor named egr-1 with the inflammatory process involved in IR injury of the lung.  We proposed that a similar association would be observed with egr-1 and IR injury in skeletal muscle. Microarray analysis of muscle specimens demonstrated 104 times upregulation of egr-1 mRNA following 4 hours of ischemia and 1 hour of reperfusion when compared to non-ischemic muscles. Thus, egr-1 protein upregulation was confirmed by Western blot analysis and time course for egr-1 upregulation during reperfusion established. The graph below demonstrates that egr-1 upregulation was highest during ischemia and that expression declined to baseline following the first 2 hours of reperfusion.

These findings encourage further research involving role of egr-1 in IR injury.