The transcriptional expression of an
ischemia responsive
protein (irp94) in the hippocampus of rats was analyzed by Northern blotting. A transient forebrain
ischemia was induced in the rats by temporary occluding of the bilateral common carotid arteries (CCAs) for various periods, and then reperfusion. Among the frontal, parietal, temporal and occipital lobes, and the cerebellum and hippocampus, the maximum
mRNA expression of irp94 was at the occipital lobe, and the minimum was at the parietal lobe following ten min of forebrain
ischemia. The irp94
mRNA expression reached a maximum fifteen min after the transient
ischemia. From twenty min on after the
ischemia its expression decreased. After a ten-min
ischemia and the following reperfusion, irp94
mRNA expression gradually increased in the first twelve h, and then decreased. The expression pattern was like that of the endoplasmic reticulum chaperone,
Erp72, but not that of the cytosol chaperone, hsp72. In addition, when intracellular
ATP was depleted with
antimycin A the
mRNA level of irp94 increased in a thyrocyte cell culture model. The results suggest that irp94, like a
molecular chaperone, may play a role in protecting the cell against external stimulation, especially after a transient forebrain
ischemia. Although future studies of irp94 will be required to clarify the interactions with other intracellular factors inducing
ischemia or showing
molecular chaperone activity, what is offered here is an insight into its functional role as a component of stress response in neurons that should be considered as a new therapeutic approach for the treatment of
ischemia.