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Overexpression of UCP2 protects thalamic neurons following global ischemia in the mouse.

Deierborg Olsson, Tomas ; Wieloch, Tadeusz LU ; Diano, Sabrina ; Warden, Craig H ; Horvath, Tamas L and Mattiasson, Gustav LU (2008) In Journal of Cerebral Blood Flow and Metabolism 28. p.1186-1195
Abstract
Uncoupling protein 2 (UCP2) is upregulated in the brain after sublethal ischemia, and overexpression of UCP2 is neuroprotective in several models of neurodegenerative disease. We investigated if increased levels of UCP2 diminished neuronal damage after global brain ischemia by subjecting mice overexpressing UCP2 (UCP2/3tg) and wild-type littermates (wt) to a 12-min global ischemia. The histopathological outcome in the cortex, hippocampus, striatum, and thalamus was evaluated at 4 days of recovery, allowing maturation of the selective neuronal death. Global ischemia led to extensive cell death in the striatum, thalamus, and in the CA1 and CA2, and less-pronounced cell death in the CA3 and dentate gyrus (DG) hippocampal subfields. Histologic... (More)
Uncoupling protein 2 (UCP2) is upregulated in the brain after sublethal ischemia, and overexpression of UCP2 is neuroprotective in several models of neurodegenerative disease. We investigated if increased levels of UCP2 diminished neuronal damage after global brain ischemia by subjecting mice overexpressing UCP2 (UCP2/3tg) and wild-type littermates (wt) to a 12-min global ischemia. The histopathological outcome in the cortex, hippocampus, striatum, and thalamus was evaluated at 4 days of recovery, allowing maturation of the selective neuronal death. Global ischemia led to extensive cell death in the striatum, thalamus, and in the CA1 and CA2, and less-pronounced cell death in the CA3 and dentate gyrus (DG) hippocampal subfields. Histologic damage was significantly lower in the ventral posterolateral VPL and medial VPM thalamic nuclei in UCP2/3tg animals compared with wt. These thalamic regions showed a larger increase in UCP2 expression in UCP2/3tg compared with wt animals relative to the nonprotected DG. In the other regions studied, the histologic damage was lower or equal in UCP2/3tg animals compared with wt. Consequently, neuroprotection in the thalamus correlated with a high expression of UCP2, which is neuroprotective in a number of models of neurodegenerative diseases.Journal of Cerebral Blood Flow & Metabolism advance online publication, 27 February 2008; doi:10.1038/jcbfm.2008.8. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Cerebral Blood Flow and Metabolism
volume
28
pages
1186 - 1195
publisher
Nature Publishing Group
external identifiers
  • pmid:18301432
  • wos:000256116700011
  • scopus:44349154324
ISSN
1559-7016
DOI
10.1038/jcbfm.2008.8
language
English
LU publication?
yes
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The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Laboratory for Experimental Brain Research (013041000)
id
66022f89-ce37-43e8-a42b-5600c7a363d6 (old id 1041489)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/18301432?dopt=Abstract
date added to LUP
2016-04-04 09:40:06
date last changed
2022-02-13 18:25:40
@article{66022f89-ce37-43e8-a42b-5600c7a363d6,
  abstract     = {{Uncoupling protein 2 (UCP2) is upregulated in the brain after sublethal ischemia, and overexpression of UCP2 is neuroprotective in several models of neurodegenerative disease. We investigated if increased levels of UCP2 diminished neuronal damage after global brain ischemia by subjecting mice overexpressing UCP2 (UCP2/3tg) and wild-type littermates (wt) to a 12-min global ischemia. The histopathological outcome in the cortex, hippocampus, striatum, and thalamus was evaluated at 4 days of recovery, allowing maturation of the selective neuronal death. Global ischemia led to extensive cell death in the striatum, thalamus, and in the CA1 and CA2, and less-pronounced cell death in the CA3 and dentate gyrus (DG) hippocampal subfields. Histologic damage was significantly lower in the ventral posterolateral VPL and medial VPM thalamic nuclei in UCP2/3tg animals compared with wt. These thalamic regions showed a larger increase in UCP2 expression in UCP2/3tg compared with wt animals relative to the nonprotected DG. In the other regions studied, the histologic damage was lower or equal in UCP2/3tg animals compared with wt. Consequently, neuroprotection in the thalamus correlated with a high expression of UCP2, which is neuroprotective in a number of models of neurodegenerative diseases.Journal of Cerebral Blood Flow & Metabolism advance online publication, 27 February 2008; doi:10.1038/jcbfm.2008.8.}},
  author       = {{Deierborg Olsson, Tomas and Wieloch, Tadeusz and Diano, Sabrina and Warden, Craig H and Horvath, Tamas L and Mattiasson, Gustav}},
  issn         = {{1559-7016}},
  language     = {{eng}},
  pages        = {{1186--1195}},
  publisher    = {{Nature Publishing Group}},
  series       = {{Journal of Cerebral Blood Flow and Metabolism}},
  title        = {{Overexpression of UCP2 protects thalamic neurons following global ischemia in the mouse.}},
  url          = {{http://dx.doi.org/10.1038/jcbfm.2008.8}},
  doi          = {{10.1038/jcbfm.2008.8}},
  volume       = {{28}},
  year         = {{2008}},
}