Stroke, Vol 24, 2121-2127, Copyright © 1993 by American Heart Association
K Kogure and H Kato
BACKGROUND: Using the techniques of molecular biology, recent experimental
studies have shown that cerebral ischemia induces a variety of changes in
gene expression in the brain. SUMMARY OF REVIEW: During the early
postischemic stages, protein synthesis in the brain is generally
suppressed, but specific genes are expressed and their corresponding
proteins may be synthesized, such as immediate-early gene products (c-fos,
c-jun, and zinc finger gene), heat-shock proteins, and amyloid precursor
protein. The ability of neurons to induce such stress responses, which
depends on both the severity of ischemia and the intrinsic nature of the
neuronal populations, may be directly associated with neuronal death and
survival after ischemia. Nerve growth factor and fibroblast growth factor
are also induced after ischemia and may be related to repair processes, in
which a role of glial cells is suggested. Postischemic events that may be
associated with the altered gene expression include (1) induction of
tolerance to ischemia after pretreatment with sublethal ischemia, (2) slow,
progressive neuronal changes and the development of neuronal plasticity
after ischemia, and (3) delayed neuronal changes in remote areas outside
the cerebral ischemic focus. CONCLUSIONS: Because a variety of harmful
stresses, including ischemia, elicit the same stress response and because
this response is induced when total protein synthesis in the brain is
nearly completely suppressed, this response may be vital to cell survival
and repair. A successful induction of this response may induce resistance
and survival of neurons after ischemia. However, failure or abortion of the
response and persistent stresses may lead to neuronal death and possibly
long-term changes and degeneration.
ARTICLES
Altered gene expression in cerebral ischemia
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.
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