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Related Experiment Videos

Early decrease of apurinic/apyrimidinic endonuclease expression after transient focal cerebral ischemia in mice.

M Fujimura1, Y Morita-Fujimura, M Kawase

  • 1Department of Neurosurgery, Stanford University School of Medicine, Palo Alto, California 94304, USA.

Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism
|May 18, 1999
PubMed
Summary

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A rapid decrease in apurinic/apyrimidinic endonuclease (APE/Ref-1) occurs after transient focal ischemia in mice. This reduction precedes DNA fragmentation, suggesting a role in brain cell death following stroke.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Apurinic/apyrimidinic endonuclease (APE/Ref-1) is crucial for DNA base excision repair.
  • APE/Ref-1 is a multifunctional protein involved in DNA repair and gene regulation.
  • Transient focal ischemia can lead to significant cellular damage in the brain.

Purpose of the Study:

  • To investigate the changes in APE/Ref-1 protein expression following transient focal ischemia in a mouse model.
  • To determine if APE/Ref-1 reduction precedes DNA fragmentation and subsequent cell death.

Main Methods:

  • Transient focal ischemia was induced in mice.
  • Immunohistochemistry was used to assess APE/Ref-1 nuclear expression in brain tissue.
  • Western blot analysis quantified APE/Ref-1 protein levels.

Related Experiment Videos

  • DNA fragmentation was evaluated at different time points post-ischemia.

    • Main Results:

    • Nuclear APE/Ref-1 expression decreased rapidly (within 5 minutes) in the ischemic core after 60 minutes of ischemia.
    • A significant reduction in APE/Ref-1-positive cells was observed throughout the middle cerebral artery territory.
    • Western blot confirmed a reduction in the 37-kDa APE/Ref-1 band after ischemia.
    • Significant DNA fragmentation was detected at 24 hours, but not at 4 hours, post-ischemia.

    Conclusions:

    • APE/Ref-1 levels decrease rapidly following transient focal ischemia in mice.
    • This reduction in APE/Ref-1 occurs before the peak of DNA fragmentation, suggesting a potential role in the pathogenesis of ischemic brain injury.
    • The findings suggest that impaired DNA repair due to decreased APE/Ref-1 may contribute to necrosis and apoptosis after transient focal ischemia.