Early c-Fos Induction after Cerebral Ischemia: A Possible Neuroprotective Role

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  • Sunghee Cho
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University at W. M. Burke Medical Research Institute, White Plains, New York, U.S.A.
  • Eun-Mi Park
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University at W. M. Burke Medical Research Institute, White Plains, New York, U.S.A.
  • Yoonseong Kim
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University at W. M. Burke Medical Research Institute, White Plains, New York, U.S.A.
  • Nian Liu
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University at W. M. Burke Medical Research Institute, White Plains, New York, U.S.A.
  • Judit Gal
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University at W. M. Burke Medical Research Institute, White Plains, New York, U.S.A.
  • Bruce T. Volpe
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University at W. M. Burke Medical Research Institute, White Plains, New York, U.S.A.
  • Tong H. Joh
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University at W. M. Burke Medical Research Institute, White Plains, New York, U.S.A.

抄録

<jats:p> The role of c-Fos in neurodegeneration or neuroprotection after cerebral ischemia is controversial. To investigate whether early c-Fos induction after ischemia is associated with neuroprotection, rats were subjected to 10 minutes of transient forebrain ischemia and c-Fos expression was examined. Resistant dentate granule cells and neurons in CA2–4 displayed more robust immunoreactivity than vulnerable neurons in the CA1 region of hippocampus during early hours of reperfusion. By 6 hours after reperfusion, c-Fos immunoreactivity was greatly diminished in all areas of the hippocampus. Administration of N-acetyl-O-methyldopamine (NAMDA), a compound previously shown to protect CA1 neurons against ischemia, increased c-Fos immunoreactivity in the CA1 vulnerable region at 6 hours after ischemia and protected SK-N-BE(2)C neurons from oxygen glucose deprivation. Further in vitro study showed that NAMDA potentiated phorbol-12 myristate-13 acetate (PMA)-induced c-Fos expression, AP1 binding activity, and late gene expression determined by chloramphenicol acetyltransferase (CAT) activity from AP1 containing tyrosine hydroxylase promoter-CAT fusion gene in SK-N-BE(2)C neurons. In vivo and in vitro results showed that a neuroprotectant, NAMDA, in concert with another stimulus (for example, ischemia or PMA) up-regulates c-Fos expression and suggested that the early rise of NAMDA-induced c-Fos expression in vulnerable CA1 neurons may account for neuroprotection by means of up-regulating late gene expression for survival. </jats:p>

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