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The asparaginyl endopeptidase legumain after experimental stroke.

Ishizaki, Taku; Erickson, Agnes LU ; Kuric, Enida LU ; Shamloo, Mehrdad; Hara-Nishimura, Ikuko; Inacio, Ana LU ; Wieloch, Tadeusz LU and Ruscher, Karsten LU (2010) In Journal of Cerebral Blood Flow and Metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism Apr 7. p.1756-1766
Abstract
Various proteases in the brain contribute to ischemic brain injury. We investigated the involvement of the asparaginyl endopeptidase legumain after experimental stroke. On the basis of gene array studies and in situ hybridizations, we observed an increase of legumain expression in the peri-infarct area of rats after transient occlusion of the middle cerebral artery (MCAO) for 120 mins with a maximum expression at 24 and 48 h. Immunohistochemical analyses revealed the expression of legumain in Iba1(+) microglial cells and glial fibrillary acidic protein-positive astrocytes of the peri-infarct area in mice after MCAO. Post-stroke recovery was also studied in aged legumain-deficient mice (45 to 58 weeks old). Legumain-deficient mice did not... (More)
Various proteases in the brain contribute to ischemic brain injury. We investigated the involvement of the asparaginyl endopeptidase legumain after experimental stroke. On the basis of gene array studies and in situ hybridizations, we observed an increase of legumain expression in the peri-infarct area of rats after transient occlusion of the middle cerebral artery (MCAO) for 120 mins with a maximum expression at 24 and 48 h. Immunohistochemical analyses revealed the expression of legumain in Iba1(+) microglial cells and glial fibrillary acidic protein-positive astrocytes of the peri-infarct area in mice after MCAO. Post-stroke recovery was also studied in aged legumain-deficient mice (45 to 58 weeks old). Legumain-deficient mice did not show any differences in physiologic parameters compared with respective littermates before, during MCAO (45 mins), and the subsequent recovery period of 8 days. Moreover, legumain deficiency had no effect on mortality, infarct volume, and the neurologic deficit determined by the rotating pole test, a standardized grip strength test, and the pole test. However, a reduced number of invading CD74(+) cells in the ischemic hemisphere indicates an involvement in post-stroke inflammation. We conclude that legumain is not essential for the functional deficit after MCAO but may be involved in mechanisms of immune cell invasion.Journal of Cerebral Blood Flow & Metabolism advance online publication, 17 March 2010; doi:10.1038/jcbfm.2010.39. (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
Apr 7
pages
1756 - 1766
publisher
Nature Publishing Group
external identifiers
  • WOS:000282382200009
  • PMID:20234379
  • Scopus:77957695468
ISSN
1559-7016
DOI
10.1038/jcbfm.2010.39
language
English
LU publication?
yes
id
7cb46d8d-093c-44e0-adf4-79be9a1be38f (old id 1582009)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/20234379?dopt=Abstract
date added to LUP
2010-04-07 17:05:46
date last changed
2016-11-10 16:41:01
@misc{7cb46d8d-093c-44e0-adf4-79be9a1be38f,
  abstract     = {Various proteases in the brain contribute to ischemic brain injury. We investigated the involvement of the asparaginyl endopeptidase legumain after experimental stroke. On the basis of gene array studies and in situ hybridizations, we observed an increase of legumain expression in the peri-infarct area of rats after transient occlusion of the middle cerebral artery (MCAO) for 120 mins with a maximum expression at 24 and 48 h. Immunohistochemical analyses revealed the expression of legumain in Iba1(+) microglial cells and glial fibrillary acidic protein-positive astrocytes of the peri-infarct area in mice after MCAO. Post-stroke recovery was also studied in aged legumain-deficient mice (45 to 58 weeks old). Legumain-deficient mice did not show any differences in physiologic parameters compared with respective littermates before, during MCAO (45 mins), and the subsequent recovery period of 8 days. Moreover, legumain deficiency had no effect on mortality, infarct volume, and the neurologic deficit determined by the rotating pole test, a standardized grip strength test, and the pole test. However, a reduced number of invading CD74(+) cells in the ischemic hemisphere indicates an involvement in post-stroke inflammation. We conclude that legumain is not essential for the functional deficit after MCAO but may be involved in mechanisms of immune cell invasion.Journal of Cerebral Blood Flow & Metabolism advance online publication, 17 March 2010; doi:10.1038/jcbfm.2010.39.},
  author       = {Ishizaki, Taku and Erickson, Agnes and Kuric, Enida and Shamloo, Mehrdad and Hara-Nishimura, Ikuko and Inacio, Ana and Wieloch, Tadeusz and Ruscher, Karsten},
  issn         = {1559-7016},
  language     = {eng},
  pages        = {1756--1766},
  publisher    = {ARRAY(0x961b108)},
  series       = {Journal of Cerebral Blood Flow and Metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism},
  title        = {The asparaginyl endopeptidase legumain after experimental stroke.},
  url          = {http://dx.doi.org/10.1038/jcbfm.2010.39},
  volume       = {Apr 7},
  year         = {2010},
}