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Common patterns of bcl-2 family gene expression in two traumatic brain injury models
Journal article   Open access   Peer reviewed

Common patterns of bcl-2 family gene expression in two traumatic brain injury models

Kenneth I Strauss, Raj K Narayan and Ramesh Raghupathi
Neurotoxicity research, v 6(4), pp 333-342
2004
PMID: 15545017
url
https://doi.org/10.1007/BF03033444View
Published, Version of Record (VoR) Open

Abstract

bcl-X Protein Multigene Family RNA, Messenger - genetics Gene Expression Regulation - physiology Rats Male Brain Injuries - genetics Brain Injuries - metabolism bcl-2-Associated X Protein Proto-Oncogene Proteins c-bcl-2 - biosynthesis Rats, Sprague-Dawley RNA, Messenger - biosynthesis Animals Time Factors Proto-Oncogene Proteins c-bcl-2 - genetics Disease Models, Animal
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. Anti-cell 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.

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Neurosciences
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