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Photochemical brain injury in rats triggers DNA fragmentation, p53 and HSP72.

Authors
  • Manev, H
  • Kharlamov, A
  • Armstrong, D M
Type
Published Article
Journal
Neuroreport
Publisher
Ovid Technologies (Wolters Kluwer) - Lippincott Williams & Wilkins
Publication Date
Dec 20, 1994
Volume
5
Issue
18
Pages
2661–2664
Identifiers
PMID: 7696627
Source
Medline
License
Unknown

Abstract

The aim of the study was to examine whether apoptosis, apoptosis-related protein p53 and heat-shock protein (HSP) 72 participate in the response of the brain to focal injury. Male Sprague-Dawley rats received intravenously a photosensitive dye rose bengal. Unilateral cortical thrombosis was induced by illuminating the skull of rose bengal-treated rats for 10 min with a focused beam of light. Animals were killed and brains were processed for immunohistochemical detection of DNA fragmentation, p53, and HSP72 kD. DNA fragmentation and p53 were increased only in the perifocal area in the cortex ipsilateral to the thrombotic focus, while HSP72 increased throughout the ipsilateral cortex, except in the immediate perifocal area. The results suggest that in response to focal brain injury, some cells die through an apoptotic process that might involve an accumulation of p53.

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