| pubmed-article:15241180 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15241180 | lifeskim:mentions | umls-concept:C0225336 | lld:lifeskim |
| pubmed-article:15241180 | lifeskim:mentions | umls-concept:C0228174 | lld:lifeskim |
| pubmed-article:15241180 | lifeskim:mentions | umls-concept:C0007587 | lld:lifeskim |
| pubmed-article:15241180 | lifeskim:mentions | umls-concept:C0623362 | lld:lifeskim |
| pubmed-article:15241180 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:15241180 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:15241180 | pubmed:dateCreated | 2004-7-8 | lld:pubmed |
| pubmed-article:15241180 | pubmed:abstractText | Matrix metalloproteinases (MMPs) may contribute to the pathophysiology of cerebral ischemia by degrading matrix components in the neurovascular unit. In this study, the authors document a pathway by which MMPs interfere with cell-matrix interactions and trigger caspase-mediated cytotoxicity in brain endothelial cells. Hypoxia-reoxygenation induced endothelial cytotoxicity. Cytoprotection with zDEVD-fmk confirmed that cell death was partly caspase mediated. The temporal profile of caspase-3 activation was matched by elevations in MMP-2 and MMP-9. MMP inhibitors significantly decreased caspase-3 activation and reduced endothelial cell death. Degradation of matrix fibronectin confirmed the presence of extracellular proteolysis. Increasing integrin-linked kinase signaling with the beta1 integrin-activating antibody (8A2) ameliorated endothelial cytotoxicity. The results suggest that MMP-9 and MMP-2 contribute to caspase-mediated brain endothelial cell death after hypoxia-reoxygenation by disrupting cell-matrix interactions and homeostatic integrin signaling. | lld:pubmed |
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| pubmed-article:15241180 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15241180 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15241180 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15241180 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15241180 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:15241180 | pubmed:issn | 0271-678X | lld:pubmed |
| pubmed-article:15241180 | pubmed:author | pubmed-author:LoEng HEH | lld:pubmed |
| pubmed-article:15241180 | pubmed:author | pubmed-author:LeeSun-RyungS... | lld:pubmed |
| pubmed-article:15241180 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15241180 | pubmed:volume | 24 | lld:pubmed |
| pubmed-article:15241180 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15241180 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15241180 | pubmed:pagination | 720-7 | lld:pubmed |
| pubmed-article:15241180 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:15241180 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15241180 | pubmed:articleTitle | Induction of caspase-mediated cell death by matrix metalloproteinases in cerebral endothelial cells after hypoxia-reoxygenation. | lld:pubmed |
| pubmed-article:15241180 | pubmed:affiliation | Neuroprotection Research Laboratory, Department of Neurology, Massachusetts General Hospital, and Program in Neuroscience, Harvard Medical School, Charlestown, Massachusetts 02129, USA. | lld:pubmed |
| pubmed-article:15241180 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15241180 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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