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Increase in p53 protein expression following cortical infarction in the spontaneously hypertensive rat

H Watanabe1, S Ohta, Y Kumon

  • 1Department of Neurological Surgery, Ehime University School of Medicine, Shigenobu-cho, Onsen-gun, 791-0295 Ehime, Japan.

Brain Research
|August 6, 1999
PubMed

Insights

Wild type p53 (wt-p53) protein expression and DNA fragmentation in brain neurons were studied after stroke in rats. Findings suggest wt-p53 dependent neuronal death contributes to stroke injury severity.

Area of Science:

  • Neuroscience
  • Pathology

Background:

  • Cerebral ischemia, a leading cause of stroke, results in neuronal damage and death.
  • The role of p53 protein in the neuronal cell death following ischemic stroke requires further elucidation.

Purpose of the Study:

  • To investigate the expression of wild type p53 (wt-p53) and mutant type p53 (mt-p53) proteins.
  • To examine the occurrence of DNA fragmentation in cerebral neurons after middle cerebral artery occlusion (MCAO).

Main Methods:

  • Stroke-prone spontaneously hypertensive (SH-SP) rats underwent permanent middle cerebral artery occlusion (MCAO).
  • Terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL staining) was used to detect DNA fragmentation.
  • Immunoreactivity for wt-p53 and mt-p53 proteins was assessed in cortical neurons.

Main Results:

  • TUNEL staining revealed significant nuclear staining in neurons surrounding the ischemic core three days post-MCAO.
  • Wt-p53 immunoreactivity was detected in cortical neurons on the lesioned side one day after MCAO, co-localizing with TUNEL staining.
  • No mt-p53 immunoreactivity was observed at any time point after MCAO.

Conclusions:

  • Wt-p53 dependent neuronal cell death occurs in the ischemic periphery following cerebral ischemia.
  • The wt-p53 pathway may play a significant role in exacerbating cerebral ischemic injury.
  • Targeting wt-p53 mediated cell death could be a potential therapeutic strategy for stroke.

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