Apoptosis after traumatic human spinal cord injury

Evelyne Emery, Philipp Aldana, Mary B Bunge, William Puckett, Anu Srinivasan, Robert W. Keane, John Bethea, Allan D O Levi

Research output: Contribution to journalArticle

356 Citations (Scopus)

Abstract

Object. Apoptosis is a form of programmed cell death seen in a variety of developmental and disease states, including traumatic injuries. The main objective of this study was to determine whether apoptosis is observed after human spinal cord injury (SCI). The spatial and temporal expression of apoptotic cells as well as the nature of the cells involved in programmed cell death were also investigated. Methods. The authors examined the spinal cords of 15 patients who died between 3 hours and 2 months after a traumatic Sci. Apoptotic cells were found at the edges of the lesion epicenter and in the adjacent white matter, particularly in the ascending tracts, by using histological (cresyl violet, hematoxylin and eosin) and nuclear staining (Hoechst 33342). The presence of apoptotic cells was supported by staining with the terminal deoxynucleotidyl transferase-mediated deoxyuridinetriphosphate nick-end labeling technique and confirmed by immunostaining for the processed form of caspase-3 (cpp-32), a member of the interleukin- 1β-converting enzyme/Caenorhabditis elegans D 3 (ICE/CED-3) family of proteases that plays an essential role in programmed cell death. Apoptosis in this series of human SCIs was a prominent pathological finding in 14 of the 15 spinal cords examined when compared with five uninjured control spinal cords. To determine the type of cells undergoing apoptosis, the authors immunostained specimens with a variety of antibodies, including glial fibrillary acidic protein, 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNPase), and CD45/68. Oligodendrocytes stained with CNPase and a number of apoptotic nuclei colocalized with positive staining for this antibody. Conclusions. These results support the hypothesis that apoptosis occurs in human SCIs and is accompanied by the activation of caspase-3 of the cysteine protease family. This mechanism of celt death contributes to the secondary injury processes seen after human SCI and may have important clinical implications for the further development of protease inhibitors to prevent programmed cell death.

Original languageEnglish
Pages (from-to)911-920
Number of pages10
JournalJournal of Neurosurgery
Volume89
Issue number6
StatePublished - Dec 1 1998

Fingerprint

Spinal Cord Injuries
nucleotidase
Apoptosis
Cell Death
Spinal Cord
Cyclic Nucleotides
Staining and Labeling
Caspase 3
Caspase 1
Cysteine Proteases
DNA Nucleotidylexotransferase
Antibodies
Glial Fibrillary Acidic Protein
Oligodendroglia
Caenorhabditis elegans
Wounds and Injuries
Hematoxylin
Eosine Yellowish-(YS)
Protease Inhibitors
Peptide Hydrolases

Keywords

  • Apoptosis
  • Caspase-3
  • Human spinal cord injury

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Cite this

Emery, E., Aldana, P., Bunge, M. B., Puckett, W., Srinivasan, A., Keane, R. W., ... Levi, A. D. O. (1998). Apoptosis after traumatic human spinal cord injury. Journal of Neurosurgery, 89(6), 911-920.

Apoptosis after traumatic human spinal cord injury. / Emery, Evelyne; Aldana, Philipp; Bunge, Mary B; Puckett, William; Srinivasan, Anu; Keane, Robert W.; Bethea, John; Levi, Allan D O.

In: Journal of Neurosurgery, Vol. 89, No. 6, 01.12.1998, p. 911-920.

Research output: Contribution to journalArticle

Emery, E, Aldana, P, Bunge, MB, Puckett, W, Srinivasan, A, Keane, RW, Bethea, J & Levi, ADO 1998, 'Apoptosis after traumatic human spinal cord injury', Journal of Neurosurgery, vol. 89, no. 6, pp. 911-920.
Emery E, Aldana P, Bunge MB, Puckett W, Srinivasan A, Keane RW et al. Apoptosis after traumatic human spinal cord injury. Journal of Neurosurgery. 1998 Dec 1;89(6):911-920.
Emery, Evelyne ; Aldana, Philipp ; Bunge, Mary B ; Puckett, William ; Srinivasan, Anu ; Keane, Robert W. ; Bethea, John ; Levi, Allan D O. / Apoptosis after traumatic human spinal cord injury. In: Journal of Neurosurgery. 1998 ; Vol. 89, No. 6. pp. 911-920.
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