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 Citations (Scopus)

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

Fingerprint

Short Interspersed Nucleotide Elements
Organism Cloning
Ischemia
Brain
Cell Death
Gerbillinae
Hippocampus
Central Nervous System
Neurons

Keywords

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

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Cloning and expression of short interspersed elements B1 and B2 in ischemic brain. / Kalkkila, Juha Pekka; Sharp, Frank R; Kärkkäinen, Iivari; Reilly, Melinda; Lu, Aigang; Solway, Karen; Murrel, Matt; Honkaniemi, Jari.

In: European Journal of Neuroscience, Vol. 19, No. 5, 03.2004, p. 1199-1206.

Research output: Contribution to journalArticle

Kalkkila, JP, Sharp, FR, 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, vol. 19, no. 5, pp. 1199-1206. https://doi.org/10.1111/j.1460-9568.2004.03233.x
Kalkkila, Juha Pekka ; Sharp, Frank R ; Kärkkäinen, Iivari ; Reilly, Melinda ; Lu, Aigang ; Solway, Karen ; Murrel, Matt ; Honkaniemi, Jari. / Cloning and expression of short interspersed elements B1 and B2 in ischemic brain. In: European Journal of Neuroscience. 2004 ; Vol. 19, No. 5. pp. 1199-1206.
@article{ccdc5940ed3c44ac9c1c154e3779da72,
title = "Cloning and expression of short interspersed elements B1 and B2 in ischemic brain",
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.",
keywords = "Alu, Apoptosis, Gerbil, Pol III, Retrotransposon, Stress",
author = "Kalkkila, {Juha Pekka} and Sharp, {Frank R} and Iivari K{\"a}rkk{\"a}inen and Melinda Reilly and Aigang Lu and Karen Solway and Matt Murrel and Jari Honkaniemi",
year = "2004",
month = "3",
doi = "10.1111/j.1460-9568.2004.03233.x",
language = "English (US)",
volume = "19",
pages = "1199--1206",
journal = "European Journal of Neuroscience",
issn = "0953-816X",
publisher = "Wiley-Blackwell",
number = "5",

}

TY - JOUR

T1 - Cloning and expression of short interspersed elements B1 and B2 in ischemic brain

AU - Kalkkila, Juha Pekka

AU - Sharp, Frank R

AU - Kärkkäinen, Iivari

AU - Reilly, Melinda

AU - Lu, Aigang

AU - Solway, Karen

AU - Murrel, Matt

AU - Honkaniemi, Jari

PY - 2004/3

Y1 - 2004/3

N2 - 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.

AB - 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.

KW - Alu

KW - Apoptosis

KW - Gerbil

KW - Pol III

KW - Retrotransposon

KW - Stress

UR - http://www.scopus.com/inward/record.url?scp=1642307859&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=1642307859&partnerID=8YFLogxK

U2 - 10.1111/j.1460-9568.2004.03233.x

DO - 10.1111/j.1460-9568.2004.03233.x

M3 - Article

C2 - 15016078

AN - SCOPUS:1642307859

VL - 19

SP - 1199

EP - 1206

JO - European Journal of Neuroscience

JF - European Journal of Neuroscience

SN - 0953-816X

IS - 5

ER -