rdf:type |
|
lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0025543,
umls-concept:C0025914,
umls-concept:C0026809,
umls-concept:C0027746,
umls-concept:C0185117,
umls-concept:C0205250,
umls-concept:C0332307,
umls-concept:C0333735,
umls-concept:C0596901,
umls-concept:C0927232,
umls-concept:C1417203,
umls-concept:C1618608,
umls-concept:C2911684
|
pubmed:issue |
3
|
pubmed:dateCreated |
2000-10-18
|
pubmed:abstractText |
Reactive astrocytes occurring in response to neurodegeneration are thought to play an important role in neuronal regeneration by upregulating the expression of extracellular matrix (ECM) components as well as the ECM degrading metalloproteinases (MMPs). We examined the mRNA levels and cellular distribution of membrane type matrix metalloproteinase 1 (MT1-MMP) and tissue inhibitors 1-4 of MMPs (TIMPs) in brain stem and spinal cord of wobbler (WR) mutant mice affected by progressive neurodegeneration and astrogliosis. MT1-MMP, TIMP-1 and TIMP-3 mRNA levels were elevated, whereas TIMP-2 and TIMP-4 expression was not affected. MT1-MMP was expressed in reactive astrocytes of WR. In primary astrocyte cultures, MT1-MMP mRNA was upregulated by exogeneous tumor necrosis factor alpha. Increased plasma membrane and secreted MMP activities were found in primary WR astrocytes.
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pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Matrix Metalloproteinase 14,
http://linkedlifedata.com/resource/pubmed/chemical/Matrix Metalloproteinases...,
http://linkedlifedata.com/resource/pubmed/chemical/Metalloendopeptidases,
http://linkedlifedata.com/resource/pubmed/chemical/Mmp14 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Tissue Inhibitor of...,
http://linkedlifedata.com/resource/pubmed/chemical/Tissue Inhibitor of...,
http://linkedlifedata.com/resource/pubmed/chemical/Tissue Inhibitor of...,
http://linkedlifedata.com/resource/pubmed/chemical/Tissue Inhibitor of...,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/tissue inhibitor of...
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
|
pubmed:issn |
0014-5793
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pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
22
|
pubmed:volume |
481
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
227-34
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:11007969-Animals,
pubmed-meshheading:11007969-Astrocytes,
pubmed-meshheading:11007969-Cell Line,
pubmed-meshheading:11007969-Cells, Cultured,
pubmed-meshheading:11007969-Central Nervous System,
pubmed-meshheading:11007969-Enzyme Induction,
pubmed-meshheading:11007969-Gene Expression Regulation,
pubmed-meshheading:11007969-Matrix Metalloproteinase 14,
pubmed-meshheading:11007969-Matrix Metalloproteinases, Membrane-Associated,
pubmed-meshheading:11007969-Metalloendopeptidases,
pubmed-meshheading:11007969-Mice,
pubmed-meshheading:11007969-Mice, Inbred C57BL,
pubmed-meshheading:11007969-Mice, Neurologic Mutants,
pubmed-meshheading:11007969-Neurodegenerative Diseases,
pubmed-meshheading:11007969-RNA, Messenger,
pubmed-meshheading:11007969-Recombinant Proteins,
pubmed-meshheading:11007969-Tissue Inhibitor of Metalloproteinase-1,
pubmed-meshheading:11007969-Tissue Inhibitor of Metalloproteinase-2,
pubmed-meshheading:11007969-Tissue Inhibitor of Metalloproteinase-3,
pubmed-meshheading:11007969-Tissue Inhibitor of Metalloproteinases,
pubmed-meshheading:11007969-Tumor Necrosis Factor-alpha,
pubmed-meshheading:11007969-Up-Regulation
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pubmed:year |
2000
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pubmed:articleTitle |
Elevated expression of membrane type 1 metalloproteinase (MT1-MMP) in reactive astrocytes following neurodegeneration in mouse central nervous system.
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pubmed:affiliation |
Developmental Biology and Molecular Pathology, WY, University of Bielefeld, D-33501 Bielefeld, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|