| Matrix metalloproteinase-9 (MMP-9) expression and extracellular signal-regulated kinase 1 and 2 (ERK1/2) activation in exercise-reduced neuronal apoptosis after stroke. | |
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MedLine Citation:
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PMID: 20298757 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Exercise preconditioning has been shown to reduce neuronal damage in ischemic/reperfusion (I/R) injury. ERK1/2 signaling in injury has been thought to modulate neuroprotection. In this study, we investigated the effects of ERK1/2 activation on the expression and activity of MMP-9 and downstream neuronal apoptosis. Adult male Sprague-Dawley rats were subjected to 30min of exercise on a treadmill for 3 weeks. Stroke was induced by a 2-h middle cerebral artery (MCA) occlusion using an intraluminal filament. Apoptotic protein caspase-3 and neuronal apoptosis in cortex and striatum was determined by Western blot at 24h reperfusion and TUNEL staining at 48h reperfusion in 5 I/R injury groups: no treatment, MMP-9 inhibitor (doxycycline), pre-ischemic exercise, exercised animals undergone ERK1/2 inhibition (U0126), and dual inhibition of ERK1/2 and MMP-9 in exercised ischemic rats. Cerebral MMP-9 expression in ischemic rats with different treatment was determined at 6, 12 and 24h reperfusion by real-time PCR for mRNA, Western blot for protein and zymography for enzyme activity. Exercise preconditioning significantly (p<0.05) reduced apoptosis determined by caspase-3 and TUNEL. In non-exercised rats, doxycycline treatment had significant (p<0.05) reductions in apoptosis after I/R injury. The dual ERK1/2-MMP-9 inhibited exercised animals had significantly (p<0.05) reduced neuronal apoptosis that was similar to that seen in exercised ischemic rats. MMP-9 expression in I/R injury was significantly (p<0.05) reduced in the exercised animals as compared to non-exercised controls. When ERK1/2 was inhibited, the reduced MMP-9 expression was reversed to the level seen in the non-exercised controls. This study has suggested that exercise-induced neuroprotection in I/R injury may be mediated by MMP-9 and ERK1/2 expression, leading to a reduction in neuronal apoptosis. |
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Authors:
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Khawar Chaudhry; Ryan Rogers; Miao Guo; Qin Lai; Gunjan Goel; Brandon Liebelt; Xunming Ji; Alecia Curry; Aaron Carranza; David F Jimenez; Yuchuan Ding |
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Publication Detail:
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Type: Journal Article Date: 2010-03-16 |
Journal Detail:
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Title: Neuroscience letters Volume: 474 ISSN: 1872-7972 ISO Abbreviation: Neurosci. Lett. Publication Date: 2010 Apr |
Date Detail:
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Created Date: 2010-04-12 Completed Date: 2010-07-08 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7600130 Medline TA: Neurosci Lett Country: Ireland |
Other Details:
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Languages: eng Pagination: 109-14 Citation Subset: IM |
Copyright Information:
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Copyright 2010 Elsevier Ireland Ltd. All rights reserved. |
Affiliation:
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Department of Neurological Surgery, Wayne State University School of Medicine, Detroit, MI 48201, United States. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Analysis of Variance Animals Apoptosis / drug effects, physiology* Brain / drug effects, enzymology, pathology Butadienes / pharmacology Caspase 3 / metabolism Disease Models, Animal Doxycycline / pharmacology Enzyme Inhibitors / pharmacology Gene Expression Regulation, Enzymologic / drug effects, physiology In Situ Nick-End Labeling / methods Infarction, Middle Cerebral Artery / drug therapy, pathology, physiopathology, rehabilitation* Male Matrix Metalloproteinase 9 / metabolism* Mitogen-Activated Protein Kinase 1 / metabolism* Mitogen-Activated Protein Kinase 3 / metabolism* Nitriles / pharmacology Physical Conditioning, Animal / methods* Rats Rats, Sprague-Dawley Reperfusion / methods Time Factors |
| Chemical | |
Reg. No./Substance:
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0/Butadienes; 0/Enzyme Inhibitors; 0/Nitriles; 0/U 0126; 564-25-0/Doxycycline; EC 2.7.11.24/Mitogen-Activated Protein Kinase 1; EC 2.7.11.24/Mitogen-Activated Protein Kinase 3; EC 3.4.22.-/Caspase 3; EC 3.4.24.35/Matrix Metalloproteinase 9 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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