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Biphasic Expression of the Fos and Jun Families of Transcription Factors Following Transient Forebrain Ischaemia in the Rat. Effect of Hypothermia

Kamme, Fredrik LU ; Campbell, Kenneth LU and Wieloch, Tadeusz LU (1995) In European Journal of Neuroscience 7(10). p.2007-2016
Abstract

Transient global ischaemia induces the expression of immediate early genes. Using in situ hybridization, the expression of c‐fos, fosB, fra‐1, fra‐2, c‐jun and junB was studied after 15 min of normothermic and hypothermia (33°C) transient forebrain ischaemia in the rat, induced by common carotid occlusion combined with systemic hypotension. Two phases of induction of the immediate early genes were observed. The early phase, peaking at 1–2 h of reperfusion, was dominated by marked expression in the dentate gyrus. The second phase, with maximal expression at 12–36 h of reperfusion, was observed particularly in the vulnerable CA1 and CA3 regions. Hypothermia increased the early induction of one of the genes studied, signifying a... (More)

Transient global ischaemia induces the expression of immediate early genes. Using in situ hybridization, the expression of c‐fos, fosB, fra‐1, fra‐2, c‐jun and junB was studied after 15 min of normothermic and hypothermia (33°C) transient forebrain ischaemia in the rat, induced by common carotid occlusion combined with systemic hypotension. Two phases of induction of the immediate early genes were observed. The early phase, peaking at 1–2 h of reperfusion, was dominated by marked expression in the dentate gyrus. The second phase, with maximal expression at 12–36 h of reperfusion, was observed particularly in the vulnerable CA1 and CA3 regions. Hypothermia increased the early induction of one of the genes studied, signifying a differential effect of hypothermia upon the signal transduction mechanisms activating these genes. The late induction occurred earlier after hypothermic than after normothermic ischaemia. The early expression of immediate early genes is due to the rapid activation of cytosolic response elements caused by the ischaemic insult. We suggest that the late induction is a stress signal for activation of repair processes, analogous to the cellular response seen after UV light‐induced DMA damage. The relatively fast induction of the immediate early genes following hypothermic ischaemia may reflect a faster resumption of normal intracellular signalling, enhancing neuronal recovery.

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author
; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
apoptosis, hippocampus, immediate early genes, in situ hybridization, neuronal death, signal transduction
in
European Journal of Neuroscience
volume
7
issue
10
pages
10 pages
publisher
Wiley-Blackwell
external identifiers
  • pmid:8542058
  • scopus:0028980652
ISSN
0953-816X
DOI
10.1111/j.1460-9568.1995.tb00623.x
language
English
LU publication?
yes
id
357dcbc8-a1b8-48f8-8159-2cfec191829d
date added to LUP
2019-06-13 16:13:04
date last changed
2024-01-01 10:13:52
@article{357dcbc8-a1b8-48f8-8159-2cfec191829d,
  abstract     = {{<p>Transient global ischaemia induces the expression of immediate early genes. Using in situ hybridization, the expression of c‐fos, fosB, fra‐1, fra‐2, c‐jun and junB was studied after 15 min of normothermic and hypothermia (33°C) transient forebrain ischaemia in the rat, induced by common carotid occlusion combined with systemic hypotension. Two phases of induction of the immediate early genes were observed. The early phase, peaking at 1–2 h of reperfusion, was dominated by marked expression in the dentate gyrus. The second phase, with maximal expression at 12–36 h of reperfusion, was observed particularly in the vulnerable CA1 and CA3 regions. Hypothermia increased the early induction of one of the genes studied, signifying a differential effect of hypothermia upon the signal transduction mechanisms activating these genes. The late induction occurred earlier after hypothermic than after normothermic ischaemia. The early expression of immediate early genes is due to the rapid activation of cytosolic response elements caused by the ischaemic insult. We suggest that the late induction is a stress signal for activation of repair processes, analogous to the cellular response seen after UV light‐induced DMA damage. The relatively fast induction of the immediate early genes following hypothermic ischaemia may reflect a faster resumption of normal intracellular signalling, enhancing neuronal recovery.</p>}},
  author       = {{Kamme, Fredrik and Campbell, Kenneth and Wieloch, Tadeusz}},
  issn         = {{0953-816X}},
  keywords     = {{apoptosis; hippocampus; immediate early genes; in situ hybridization; neuronal death; signal transduction}},
  language     = {{eng}},
  month        = {{01}},
  number       = {{10}},
  pages        = {{2007--2016}},
  publisher    = {{Wiley-Blackwell}},
  series       = {{European Journal of Neuroscience}},
  title        = {{Biphasic Expression of the Fos and Jun Families of Transcription Factors Following Transient Forebrain Ischaemia in the Rat. Effect of Hypothermia}},
  url          = {{http://dx.doi.org/10.1111/j.1460-9568.1995.tb00623.x}},
  doi          = {{10.1111/j.1460-9568.1995.tb00623.x}},
  volume       = {{7}},
  year         = {{1995}},
}