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(Stroke. 1996;27:1682-1687.)
© 1996 American Heart Association, Inc.

Articles

Immediate Early Gene Expression in Response to Cerebral Ischemia

Friend or Foe?

Paul T. Akins, MD, PhD; Philip K. Liu, PhD Chung Y. Hsu, MD, PhD

the Cerebrovascular Disease Section, Department of Neurology, Washington University School of Medicine, St Louis, Mo (P.T.A., C.Y.H.); and the Division of Restorative Neurology and Human Neurobiology, Baylor College of Medicine, Houston, Tex (P.K.L.).

Background Cerebral ischemia is a potent modulator of gene expression. Immediate early genes undergo rapid induction after both global and focal cerebral ischemia. Many immediate early genes code for transcription factors. Additional genes, including those encoding for neurotrophic factors and neurotransmitter systems, are induced in a delayed fashion after cerebral ischemia. The functional significance of early and late gene regulation after cerebral ischemia requires futher investivation. These changes may be beneficial (friend) or detrimental (foe). Many of the genes are likely neuroprotective and important for recovery, but others may be involved in ischemic cell death mediated by apoptosis.

Summary of Review We review evidence that supports the hypothesis that cell death after cerebral ischemia occurs through the dual pathways of ischemic necrosis and apoptosis.

Conclusions Gene regulation, including immediate early genes, is required for programmed neuronal death after trophic factor deprivation and is predicted to be involved in apoptosis triggered by cerebral ischemia. Novel therapies following cerebral ischemia may be directed at genes mediating either recovery or apoptosis.

Key Words: apoptosis • cerebral ischemia • DNA damage • gene expression

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