Dr. DeGracia studies the mechanisms of cell death following brain ischemia and reperfusion. This clinically relevant research models brain injury that occurs following stroke or following resuscitation from cardiac arrest. The main focus of this work is the causes and consequences of reperfusion-induced inhibition of protein synthesis. Dr. DeGracia's previous work established that phosphorylation of eukaryotic initiation factor 2 alpha occurs in the reperfused brain. Further, this phosphorylation is caused by the eIF2 alpha kinase PERK. PERK activation is part of an endoplasmic reticulum stress response known as the unfolded protein response (UPR). Dr. DeGracia has investigated expression of the UPR in the reperfused brain and developed evidence that the UPR is expressed in an apparently dysfunctional fashion. Current work in the lab is assessing the role of mRNA regulation via stress granules and HuR granules in prolonged translation arrested in reperfused vulnerable neurons.
Dr. DeGracia's lab is funded by the NIH.