Ubiquitin-mediated stress response in the spinal cord after transient ischemia

Takashi Yamauchi, Masahiro Sakurai, Koji Abe, Goro Matsumiya, Yoshiki Sawa

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

BACKGROUND AND PURPOSE: Vulnerability of motor neurons in the spinal cord against ischemia is considered to play an important role in the development of delayed paraplegia after surgery of the thoracic aorta. However, the reasons for such vulnerability are not fully understood. Recently, the ubiquitin system has been reported to participate in neuronal cell death. In the present study, we investigated the expression of ubiquitin system molecules and discussed the relationship between the vulnerability and the ubiquitin system after transient ischemia in the spinal cord. METHODS: Fifteen minutes of spinal cord ischemia in rabbits was applied with the use of a balloon catheter. In this model, the spinal motor neuron shows selectively delayed neuronal death, whereas other spinal neurons such as interneurons survive. Immunohistochemical analysis and Western blotting for ubiquitin system molecules, ubiquitin, deubiquitylating enzyme (ubiquitin carboxy-terminal hydrolase 1), and ubiquitin-ligase parkin were examined. RESULTS: In cytoplasm, ubiquitin and ubiquitin carboxy-terminal hydrolase 1were strongly induced both in interneuron and motor neuron at the early stage of reperfusion, but the sustained expression was observed only in motor neuron. Parkin was induced strongly at 3 hours after the reperfusion, but the immunoreactivity returned to the sham control level at 6 hours in both neurons. In the nuclei, ubiquitin, ubiquitin carboxy-terminal hydrolase 1, and parkin were strongly induced in interneuron, whereas no upregulation of these proteins was observed in motor neuron. CONCLUSIONS: These results indicate that the vulnerability of motor neuron of the spinal cord might be partially attributed to the different response in ubiquitin-mediated stress response after transient ischemia.

Original languageEnglish
Pages (from-to)1883-1889
Number of pages7
JournalStroke
Volume39
Issue number6
DOIs
Publication statusPublished - Jun 1 2008

Fingerprint

Ubiquitin
Spinal Cord
Ischemia
Motor Neurons
Ubiquitin Thiolesterase
Spinal Cord Ischemia
Interneurons
Reperfusion
Neurons
Paraplegia
Ligases
Thoracic Aorta
Cytoplasm
Cell Death
Up-Regulation
Catheters
Western Blotting
Rabbits
Enzymes

Keywords

  • Ischemia
  • Paraplegia
  • Parkin
  • Spinal cord ischemia
  • Ubiquitin
  • UCH-L1

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Clinical Neurology
  • Advanced and Specialised Nursing
  • Medicine(all)

Cite this

Ubiquitin-mediated stress response in the spinal cord after transient ischemia. / Yamauchi, Takashi; Sakurai, Masahiro; Abe, Koji; Matsumiya, Goro; Sawa, Yoshiki.

In: Stroke, Vol. 39, No. 6, 01.06.2008, p. 1883-1889.

Research output: Contribution to journalArticle

Yamauchi, T, Sakurai, M, Abe, K, Matsumiya, G & Sawa, Y 2008, 'Ubiquitin-mediated stress response in the spinal cord after transient ischemia', Stroke, vol. 39, no. 6, pp. 1883-1889. https://doi.org/10.1161/STROKEAHA.106.455832
Yamauchi, Takashi ; Sakurai, Masahiro ; Abe, Koji ; Matsumiya, Goro ; Sawa, Yoshiki. / Ubiquitin-mediated stress response in the spinal cord after transient ischemia. In: Stroke. 2008 ; Vol. 39, No. 6. pp. 1883-1889.
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