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| Content Provider | Springer Nature Link |
|---|---|
| Author | Strauss, Kenneth I. Narayan, Raj K. Raghupathi, Ramesh |
| Copyright Year | 2004 |
| Abstract | Cell death/survival following traumatic brain injury (TBI) may be a result of alterations in the intracellular ratio of death and survival factors. Bcl-2 family genes mediate both cell survival and the initiation of cell death. Using lysate RNase protection assays, mRNA expression of the anti-cell death genes Bcl-2 and Bcl-xL, and the pro-cell death gene Bax, was evaluated following experimental brain injuries in adult male Sprague-Dawley rats. Both the lateral fluid-percussion (LFP) and the lateral controlled cortical impact (LCI) models of TBI showed similar patterns of gene expression. Anticell death bcl-2 and bcl-xL mRNAs were attenuated early and tended to remain depressed for at least 3 days after injury in the cortex and hippocampus ipsilateral to injury. Pro-cell death bax mRNA was elevated in these areas, usually following the decrease in anti-cell death genes. These common patterns of gene expression suggest an important role for Bcl-2 genes in cell death and survival in the injured brain. Understanding the regulation of these genes may facilitate the development of new therapeutic strategies for a condition that currently has no proven pharmacologic treatments. |
| Starting Page | 333 |
| Ending Page | 342 |
| Page Count | 10 |
| File Format | |
| ISSN | 10298428 |
| Journal | Neurotoxicity Research |
| Volume Number | 6 |
| Issue Number | 4 |
| e-ISSN | 14763524 |
| Language | English |
| Publisher | Springer-Verlag |
| Publisher Date | 2004-01-01 |
| Publisher Place | New York |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Apoptosis mRNA measurement Cerebral cortex Hippocampus Traumatic brain injury Animal models Gene expression patterns Neurosciences Pharmaceutical Sciences/Technology Neurology Neurochemistry Pharmacology/Toxicology Neurobiology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Neuroscience Toxicology |
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