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Cited by 453Spinal Cord Injury ResearchTraumatic Brain Injury and Neurovascular DisturbancesCell death mechanisms and regulation

The DOI matches its Crossref record; 92 of the 93 references it cites were found in a registry or an index.

Chapter 4 Cell death in models of spinal cord injury

Beattie, Michael S., Hermann, Gerlinda E., Rogers, Richard C., Bresnahan, Jacqueline C.·2002·Progress in Brain Research
DOI 10.1016/s0079-6123(02)37006-7
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Abstract

Current treatments for acute spinal cord injury are based on animal models of human spinal cord injury (SCI). These models have shown that the initial traumatic injury to cord tissue is followed by a long period of secondary injury that includes a number of cellular and biochemical cascades. These secondary injury processes are potential targets for therapies. Continued refinement of rat and mouse models of SCI, along with more detailed analyses of the biology of the lesion in these models, points to both necrotic and apoptotic mechanisms of cell death after SCI. In this chapter, we review recent evidence for long-term apoptotic death of oligodendrocytes in long tracts undergoing Wallerian degeneration following SCI. This process appears to be related closely to activation of microglial cells. It is has been thought that microglial cells might be the source of cytotoxic cytokines, such as tumor necrosis factor-alpha (TNF-alpha), that kill oligodendrocytes. However, more recent evidence in vivo suggests that TNF-alpha by itself may not induce necrosis or apoptosis in oligodendrocytes. We review data that suggests other possible pathways for apoptosis, such as the neurotrophin receptor p75 which is expressed in both neurons and oligodendrocytes after SCI in rats and mice. In addition, it appears that microglial activation and TNF-alpha may be important in acute SCI. Ninety minutes after a moderate contusion lesion, microglia are activated and surround dying neurons. In an 'atraumatic' model of SCI, we have now shown that TNF-alpha appears to greatly potentiate cell death mediated by glutamate receptors. These studies emphasize that multiple mechanisms and interactions contribute to secondary injury after SCI. Continued study of both contusion models and other new approaches to studying these mechanisms will be needed to maximize strategies for acute and chronic therapies, and for neural repair.

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Citations

Cites

Research works printed but not linked: 3

  1. Arnold, 2000, Caspase-3 inhibition is neuroprotective after spinal cord injury, J. Neurochem., 74, S73
  2. Beattie, 2000, TNF, glutamate and neurodegeneration in the rat spinal cord, Soc. Neurosci. Abstr, 26, 2279
  3. Crowe, 1995, Morphological evidence suggesting apoptotic nuclei in spinal cord injury, Soc. Neurosci. Abstr., 21, 232

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Metadata

Authors
Beattie, M. S., Hermann, G. E., Rogers, R. C., & Bresnahan, J. C.
Affiliations
The Ohio State University Wexner Medical Center (US)
Corresponding author
Beattie, Michael S.
ORCID
Venue
Progress in Brain Research
Publisher
Elsevier
Published
2002
Volume
137
Pages
37-47
ISSN
0079-6123 (ISSN-L)
DOI
10.1016/s0079-6123(02)37006-7
OpenAlex
W1527455107
Cited by
453
References
93
Citations by year
2026: 5 · 2025: 15 · 2024: 15 · 2023: 16 · 2022: 20 · 2021: 16 · 2020: 23 · 2019: 30 · 2018: 18 · 2017: 17 · 2016: 22 · 2015: 38 · 2014: 23 · 2013: 17 · 2012: 21
FWCI
38.08
Type
book chapter
Language
en
Open access
closed
Locations
  • Progress in brain research (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Ohio State University
  • National Institutes of Health
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK-52142, R01DK052142)
  • National Institute of Neurological Disorders and Stroke (NS38079, R01NS038079)
Topics
  • Health Sciences › Medicine › Clinical Neurology › Spinal Cord Injury Research
  • Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
spinal cord injury, secondary injury, cell death, apoptosis, necrosis, oligodendrocytes, Wallerian degeneration, microglial activation, TNF-α, glutamate receptors, bruising, animal models of spinal cord injury
MeSH terms
Animals, Disease Models, Animal, Necrosis, Oligodendroglia, Spinal Cord Injuries, Time Factors, Cell Death, Apoptosis, Disease Progression, Rats

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