期刊
MOLECULAR AND CELLULAR NEUROSCIENCE
卷 22, 期 1, 页码 98-106出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/S1044-7431(02)00024-6
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资金
- Biotechnology and Biological Sciences Research Council [C18365] Funding Source: Medline
The upregulation of TIMP-1 following an excitotoxic injury has recently been hypothesized to be part of a general neuronal response that mediates long-lasting changes involved in tissue reorganization and possibly neuroprotection. In this study we have shown for the first time that within hours of applying TIMP-1 in recombinant form or by adenovirus-mediated gene transfer, neurons are highly protected against excitotoxic injury. Neither TIMP-3 nor a nonsecretable form of TIMP-l protected neurons. TIMP-1 conferred highly significant protection to hippocampal cells exposed to a wide range of glutamic acid concentrations in both dissociated and organotypic hippocampal cultures. TIMP-1 did not prevent apoptotic cell death or death mediated by chemical ischemia. The observed neuroprotection may be explained by a decrease in calcium influx into neurons following stimulation with glutamate. These findings have a fundamental implication for our understanding of the physiological role of secreted TIMP-1 in the central nervous system. (C) 2003 Elsevier Science (USA). All rights reserved.
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