Journal article
Temporal Alterations in Cellular Bax:Bcl-2 Ratio following Traumatic Brain Injury in the Rat
Journal of neurotrauma, v 20(5), pp 421-435
May 2003
PMID: 12803975
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Abstract
Cell death/survival following CNS injury may be a result of alterations in the intracellular ratio of death and survival factors. Using immunohistochemistry, Western analysis and
in situ
hybridization, the expression of the anti-cell death protein, Bcl-2, and the pro-cell death protein, Bax, was evaluated following lateral fluid-percussion (FP) brain injury of moderate severity (2.3–2.6 atm) in adult male Sprague-Dawley rats. By 2 h post-injury, a marked reduction of cellular Bcl-2-immunoreactivity (IR) and a mild decrease in cellular Bax IR were observed in the temporal and occipital cortices, and in the hippocampal CA3 ipsilateral to the site of impact. These decreases in Bcl-2 and Bax IR appeared to precede the overt cell loss in these regions that was evident at 24 h. Immunoblot analysis supported the immunohistochemical data, with a modest but significant reduction in the intensities of both the Bcl-2 and Bax protein bands at 2 h (
p
< 0.05 compared to sham levels). However, the Bax:Bcl-2 ratio increased significantly at 2 h (2.28 ± 0.13) and remained elevated up to 7 days (2.05 ± 0.13) post-injury compared to sham-injured control tissue (1.62 ± 0.10,
p
< 0.05). Furthermore, cortical, but not hippocampal, levels of Bax protein increased by 25% (
p
< 0.05 compared to sham-injured controls) at 24 h post-injury, and returned to control levels by 7 days. In situ hybridization analysis of Bax mRNA revealed increased cellular grain density in the injured cortex (
p
< 0.05 compared to sham-injured brains), but not in the CA3 region of the injured hippocampus. No injury-induced changes in the expression of Bcl-2 mRNA were observed in any brain region. Taken together, these data suggest that the association between regional post-traumatic cell death and alterations in the cellular ratio of Bcl-2 and Bax may be, in part, due to alterations in mRNA and/or protein expression of the Bcl-2 family of proteins.
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Details
- Title
- Temporal Alterations in Cellular Bax:Bcl-2 Ratio following Traumatic Brain Injury in the Rat
- Creators
- RAMESH RAGHUPATHI - Department of Neurosurgery, University of Pennsylvania School of Medicine, Philadelphia, PennsylvaniaKENNETH I STRAUSS - Department of Neurosurgery, University of Cincinnati, Cincinnati, OhioCHEN ZHANG - Department of Neurosurgery, University of Pennsylvania School of Medicine, Philadelphia, PennsylvaniaSTANISLAW KRAJEWSKI - Burham Institute, La Jolla, CaliforniaJOHN C REED - Burham Institute, La Jolla, CaliforniaTRACY K McINTOSH - Department of Neurosurgery, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
- Publication Details
- Journal of neurotrauma, v 20(5), pp 421-435
- Publisher
- Mary Ann Liebert
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Neurobiology and Anatomy
- Web of Science ID
- WOS:000183096900003
- Scopus ID
- 2-s2.0-0038526424
- Other Identifier
- 991014877959304721
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- Collaboration types
- Domestic collaboration
- Web of Science research areas
- Clinical Neurology
- Critical Care Medicine
- Neurosciences