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Enriched environment reduces apolipoprotein E (ApoE) in reactive astrocytes and attenuates inflammation of the peri-infarct tissue after experimental stroke.

Ruscher, Karsten LU ; Johannesson, Emelie ; Brugiere, Elena ; Erickson, Agnes LU ; Rickhag, Mattias LU and Wieloch, Tadeusz LU (2009) In Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 29. p.1796-1805
Abstract
Apolipoprotein E (ApoE), a cholesterol transporter and an immunomodulator, is brain protective after experimental stroke and implicated in brain repair. Here, we study the involvement of ApoE in the restoration of brain function after experimental stroke, by using animal housing conditions that differentially improve recovery after occlusion of the middle cerebral artery occlusion (MCAO). We found that after MCAO the ApoE levels increased in the injured hemisphere over a 30 days recovery period. The exception was a proximal narrow peri-infarct rim, in which ApoE was solely localized in S100beta(+)/glial fibrillary acidic protein (GFAP) negative reactive astrocytes at 4 to 7 days of recovery. Enriched housing after MCAO caused a marked... (More)
Apolipoprotein E (ApoE), a cholesterol transporter and an immunomodulator, is brain protective after experimental stroke and implicated in brain repair. Here, we study the involvement of ApoE in the restoration of brain function after experimental stroke, by using animal housing conditions that differentially improve recovery after occlusion of the middle cerebral artery occlusion (MCAO). We found that after MCAO the ApoE levels increased in the injured hemisphere over a 30 days recovery period. The exception was a proximal narrow peri-infarct rim, in which ApoE was solely localized in S100beta(+)/glial fibrillary acidic protein (GFAP) negative reactive astrocytes at 4 to 7 days of recovery. Enriched housing after MCAO caused a marked decrease in ApoE levels compared with standard housing conditions, particularly in the ApoE/S100beta(+) reactive astrocytes. In addition, the levels of interleukin 1beta were lower in animals housed in an enriched environment. We propose that during the subacute phase after experimental stroke a zone for tissue reorganization with low cellular ApoE levels is formed. We conclude that the strong sensori-motor stimulation provided by enriched housing conditions mitigates the inflammatory response after stroke decreasing the level of ApoE that may contribute to the observed improvement of functional recovery.Journal of Cerebral Blood Flow & Metabolism advance online publication 22 July 2009; doi:10.1038/jcbfm.2009.96. (Less)
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Contribution to journal
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published
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in
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
volume
29
pages
1796 - 1805
publisher
Nature Publishing Group
external identifiers
  • wos:000271429500008
  • pmid:19623195
  • scopus:71949089337
  • pmid:19623195
ISSN
1559-7016
DOI
10.1038/jcbfm.2009.96
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: Experimental Brain Research (0131000120), Neurosurgery (013026000), Laboratory for Experimental Brain Research (013041000)
id
7093aaa8-0b4f-42c1-b7a4-978dad5f740f (old id 1452919)
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http://www.ncbi.nlm.nih.gov/pubmed/19623195?dopt=Abstract
date added to LUP
2016-04-04 09:33:44
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2022-01-29 18:27:11
@article{7093aaa8-0b4f-42c1-b7a4-978dad5f740f,
  abstract     = {{Apolipoprotein E (ApoE), a cholesterol transporter and an immunomodulator, is brain protective after experimental stroke and implicated in brain repair. Here, we study the involvement of ApoE in the restoration of brain function after experimental stroke, by using animal housing conditions that differentially improve recovery after occlusion of the middle cerebral artery occlusion (MCAO). We found that after MCAO the ApoE levels increased in the injured hemisphere over a 30 days recovery period. The exception was a proximal narrow peri-infarct rim, in which ApoE was solely localized in S100beta(+)/glial fibrillary acidic protein (GFAP) negative reactive astrocytes at 4 to 7 days of recovery. Enriched housing after MCAO caused a marked decrease in ApoE levels compared with standard housing conditions, particularly in the ApoE/S100beta(+) reactive astrocytes. In addition, the levels of interleukin 1beta were lower in animals housed in an enriched environment. We propose that during the subacute phase after experimental stroke a zone for tissue reorganization with low cellular ApoE levels is formed. We conclude that the strong sensori-motor stimulation provided by enriched housing conditions mitigates the inflammatory response after stroke decreasing the level of ApoE that may contribute to the observed improvement of functional recovery.Journal of Cerebral Blood Flow & Metabolism advance online publication 22 July 2009; doi:10.1038/jcbfm.2009.96.}},
  author       = {{Ruscher, Karsten and Johannesson, Emelie and Brugiere, Elena and Erickson, Agnes and Rickhag, Mattias and Wieloch, Tadeusz}},
  issn         = {{1559-7016}},
  language     = {{eng}},
  pages        = {{1796--1805}},
  publisher    = {{Nature Publishing Group}},
  series       = {{Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism}},
  title        = {{Enriched environment reduces apolipoprotein E (ApoE) in reactive astrocytes and attenuates inflammation of the peri-infarct tissue after experimental stroke.}},
  url          = {{http://dx.doi.org/10.1038/jcbfm.2009.96}},
  doi          = {{10.1038/jcbfm.2009.96}},
  volume       = {{29}},
  year         = {{2009}},
}