Expression of an HSP110 family, ischemia-responsive protein (irp94), in the rat brain after transient forebrain ischemia

The transcriptional expression of an ischemia responsive protein (irp94) in the hippocampus of rats was analyzed by Northern blotting. A transient for ebrain ischemia was induced in the rats by temporary occluding of the bilat eral common carotid arteries (CCAs) for various periods, and then reperfusi on. Among the frontal, parietal, temporal and occipital lobes, and the cere bellum and hippocampus, the maximum mRNA expression of irp94 was at the occ ipital 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 ex pression 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 reticulu m chaperone, Erp72, but not that of the cytosol chaperone, hsp72. In additi on, 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 tr ansient forebrain ischemia. Although future studies of irp94 will be requir ed to clarify the interactions with other intracellular factors inducing is chemia or showing molecular chaperone activity, what is offered here is an insight into its functional role as a component of stress response in neuro ns that should be considered as a new therapeutic approach for the treatmen t of ischemia.