Apoptosis associated genes are induced in gerbil hippocampus following global ischemia

J. Honkaniemi, S. M. Massa, Frank R Sharp

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Numerous studies have demonstrated evidence of DNA nick end-labeling and DNA laddering following cerebral ischemia. To determine whether genes directly implicated in apoptosis were induced by ischemia, the expression of bcl-2, bcl-x and ICE mRNAs were examined using oligonucleotide probes. Northern blots demonstrated induction of bcl-2 mRNA and bcl-x mRNAs in hippocampus 24 and 72 h following 5 min of global ischemia. In situ hybridization demonstrated induction of bcl-2 and bcl-x mRNAs in CA1 pyramidal neurons of hippocampus at 24 h following ischemia which decreased by 72 h. ICE-like mRNA was induced in non-neuronal cells in the CA1 region at 72 h following global ischemia. The data show that genes implicated in either protecting against or promoting programmed cell death in other systems are induced following cerebral ischemia. It is hypothesized that CA1 neuronal cell death could be accounted for by the failure of the ischemic cells to make protective proteins that protect the cells from an ischemic induced apoptotic-like cell death.

Original languageEnglish (US)
Pages (from-to)227-230
Number of pages4
JournalRestorative Neurology and Neuroscience
Volume9
Issue number4
StatePublished - 1996
Externally publishedYes

Fingerprint

Gerbillinae
Hippocampus
Ischemia
Apoptosis
Messenger RNA
Cell Death
Genes
Brain Ischemia
Single-Stranded DNA Breaks
Oligonucleotide Probes
Pyramidal Cells
Northern Blotting
In Situ Hybridization
DNA
Proteins

Keywords

  • Apoptosis
  • bcl-2
  • bcl-x
  • Cerebral ischemia
  • Hippocampus
  • ICE

ASJC Scopus subject areas

  • Neuroscience(all)
  • Neuropsychology and Physiological Psychology

Cite this

Apoptosis associated genes are induced in gerbil hippocampus following global ischemia. / Honkaniemi, J.; Massa, S. M.; Sharp, Frank R.

In: Restorative Neurology and Neuroscience, Vol. 9, No. 4, 1996, p. 227-230.

Research output: Contribution to journalArticle

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