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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2008-3-31
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pubmed:abstractText |
Elevated activities of matrix metalloproteinases (MMPs) following ischemic stroke have been shown to mediate ischemic injury as well as neurovascular remodeling. The extracellular MMP inducer (EMMPRIN) is a 58-kDa cell surface glycoprotein, which has been known to play a key regulatory role for MMP activities. The roles of EMMPRIN in stroke injury are not clearly understood. In this study, we investigated changes of EMMPRIN in a mouse model of permanent focal cerebral ischemia, and examined potential association between EMMPRIN and MMP-9 expression. Adult male CD-1 mice were subjected to permanent focal ischemia by intraluminal occlusion of the left middle cerebral artery (MCAO) under anesthesia. EMMPRIN expression was markedly upregulated in the peri-infarct area at 2-7 days after ischemia compared to the contralateral non-ischemic hemisphere by Western blot analysis. Immunofluorescent double staining demonstrated that EMMPRIN signals co-localized with vwF-positive endothelial cells and GFAP-positive peri-vascular astrocytes. In contrast, EMMPRIN signal did not co-localize with NeuN-positive neurons, or MPO-positive neutrophils. Dual fluorescent staining revealed that EMMPRIN co-localized with MMP-9. Our data also demonstrated that increased EMMPRIN expression correlated with increased MMP-9 levels in a temporal manner. In summary, we report for the first time that EMMPRIN expression was significantly increased in a mouse model of permanent focal cerebral ischemia. The spatial and temporal association between increased EMMPRIN expression and elevated MMP-9 levels suggest that EMMPRIN may modulate MMP-9 activity, and participate in neurovascular remodeling after ischemic stroke.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-10526099,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-10652425,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-10962435,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-11222998,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-12203394,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-12553375,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-12696756,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-14633669,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-15146242,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-15319264,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-15534110,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-15781323,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-16029217,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-16278864,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-16461815,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-16507143,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-16565723,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-16690896,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-16720380,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-16778084,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-16846501,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-16946160,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-16982929,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18164515-2357963
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0197-0186
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
52
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1086-91
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:18164515-Animals,
pubmed-meshheading:18164515-Antigens, CD147,
pubmed-meshheading:18164515-Astrocytes,
pubmed-meshheading:18164515-Brain,
pubmed-meshheading:18164515-Brain Infarction,
pubmed-meshheading:18164515-Brain Ischemia,
pubmed-meshheading:18164515-Disease Models, Animal,
pubmed-meshheading:18164515-Endothelial Cells,
pubmed-meshheading:18164515-Fluorescent Antibody Technique,
pubmed-meshheading:18164515-Glial Fibrillary Acidic Protein,
pubmed-meshheading:18164515-Infarction, Middle Cerebral Artery,
pubmed-meshheading:18164515-Male,
pubmed-meshheading:18164515-Matrix Metalloproteinase 9,
pubmed-meshheading:18164515-Mice,
pubmed-meshheading:18164515-Platelet Membrane Glycoproteins,
pubmed-meshheading:18164515-Up-Regulation
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pubmed:year |
2008
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pubmed:articleTitle |
Upregulation of EMMPRIN after permanent focal cerebral ischemia.
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pubmed:affiliation |
Center for Cerebrovascular Research, Department of Anesthesia and Perioperative Care, University of California, San Francisco, CA, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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