Published Online
on October 27, 2005

A more recent version of this article appeared on December 1, 2005

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Submitted on March 7, 2005
Revised on July 21, 2005
Accepted on August 18, 2005

The Role of Protein Kinase C in Cerebral Ischemic and Reperfusion Injury

Rachel Bright PhD and Daria Mochly-Rosen PhD^*

From the Stanford University School of Medicine, California.

^* To whom correspondence should be addressed. E-mail: mochly{at}stanford.edu.

Background and Purpose--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.

Summary of Review--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.

Conclusion--Examination of PKC isozyme activities during stroke demonstrates the clinical promise of PKC isozyme-specific modulators for the treatment of cerebral ischemia.

Key words: cerebral infarction • cerebral ischemia • neuroprotection

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