Cloning and expression of short interspersed elements B1 and B2 in ischemic brain

Juha Pekka Kalkkila, Frank R Sharp, Iivari Kärkkäinen, Melinda Reilly, Aigang Lu, Karen Solway, Matt Murrel, Jari Honkaniemi

Research output: Contribution to journalArticle

9 Scopus citations

Abstract

Global ischemia causes an extensive cell death 3 days after the ischemia in the CA1 region of the hippocampus, which is preceded by induction of a spectrum of genes with both neuroprotective and detrimental properties. This delayed cell death has been suggested to be mainly caused by programmed cell death. Here we applied differential display to characterize transcripts induced by global ischemia after 1 day in Mongolian gerbils, when the cells in the CA1 region are still viable, but initiating the cell death pathway. One of the cloned transcripts turned out to be a repeat sequence termed SINE B2. We also cloned the other member of the SINE family, SINE B1, and found it also to be slightly induced by ischemia in the CA1 region. The SINE repeat regions are not translated and their role in ischemia may be related the neurons' attempt to cope with decreased translational levels and/or genomic reorganization. Together with the previous data demonstrating the inducibility of the SINE transcripts using in vitro stress models, the present study shows that SINE transcripts are stress-inducible factors in the central nervous system.

Original languageEnglish (US)
Pages (from-to)1199-1206
Number of pages8
JournalEuropean Journal of Neuroscience
Volume19
Issue number5
DOIs
StatePublished - Mar 2004
Externally publishedYes

Keywords

  • Alu
  • Apoptosis
  • Gerbil
  • Pol III
  • Retrotransposon
  • Stress

ASJC Scopus subject areas

  • Neuroscience(all)

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    Kalkkila, J. P., Sharp, F. R., Kärkkäinen, I., Reilly, M., Lu, A., Solway, K., Murrel, M., & Honkaniemi, J. (2004). Cloning and expression of short interspersed elements B1 and B2 in ischemic brain. European Journal of Neuroscience, 19(5), 1199-1206. https://doi.org/10.1111/j.1460-9568.2004.03233.x