期刊
BRAIN RESEARCH
卷 977, 期 1, 页码 62-69出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/S0006-8993(03)02742-2
关键词
transient cerebral ischemia; hippocampus; matrix metalloproteinase; laminin; focal adhesion kinase
Cell adhesion to the extracellular matrix (ECM) functions as a survival factor and disruption of cell-ECM interaction can lead to cell death. Our previous study has demonstrated ischemia-induced enhancement of activity of extracellular metalloproteinases, which might result in the alteration of adhesive contact with ECM and affect the intracellular signaling pathway. The enzyme thought to play a major role in conveying survival signals from ECM to the cell interior is focal adhesion kinase (pp125(FAK)). In the present study, the temporal relation between activation of extracellular metalloproteinases (MMP-2 and MMP-9), degradation of extracellular matrix protein laminin and the expression of pp125(FAK) after 5 min of global ischemia in gerbil hippocampus were investigated. While significant activation of both investigated metalloproteinases occurred in the course of reperfusion, only changes in MMP-9 activity were correlated with degradation of laminin. These ischemia-induced extracellular events coincide temporarily with proteolytic modification of FAK protein and diminished level of its phosphorylated form, to about 50% of the initial value. These results are indicative of an involvement of ECM-pp125 FAK signaling pathway in ischemia-induced neuronal degeneration. (C) 2003 Elsevier Science B.V. All rights reserved.
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