The role of protein kinase C in cerebral ischemic and reperfusion injury.
OBJECTIVE
Stroke is a leading cause of disability and death in the United States, yet limited therapeutic options exist. The need for novel neuroprotective agents has spurred efforts to understand the intracellular signaling pathways that mediate cellular response to stroke. Protein kinase C (PKC) plays a central role in mediating ischemic and reperfusion damage in multiple tissues, including the brain. However, because of conflicting reports, it remains unclear whether PKC is involved in cell survival signaling, or mediates detrimental processes.


RESULTS
This review will examine the role of PKC activity in stroke. In particular, we will focus on more recent insights into the PKC isozyme-specific responses in neuronal preconditioning and in ischemia and reperfusion-induced stress.


CONCLUSIONS
Examination of PKC isozyme activities during stroke demonstrates the clinical promise of PKC isozyme-specific modulators for the treatment of cerebral ischemia.
Bright
Rachel
R
Stanford University School of Medicine, Stanford, CA 94305-5174, USA.
Mochly-Rosen
Daria
D
D000241:Adenosine / Q000378:metabolism; D000818:Animals; D017209:Apoptosis; D002545:Brain Ischemia / Q000150:complications / Q000201:enzymology*; D004195:Disease Models, Animal; D006801:Humans; D019194:Ischemic Preconditioning; D007527:Isoenzymes / Q000378:metabolism; D009474:Neurons / Q000201:enzymology; D011493:Protein Kinase C / Q000378:metabolism*; D015427:Reperfusion Injury / Q000150:complications / Q000201:enzymology*; D015854:Up-Regulation
D007527:Isoenzymes; D011493:Protein Kinase C; D000241:Adenosine