title: Endoplasmic reticulum stress induced in motor neurons by transient spinal cord ischemia in rabbits.
abstract: OBJECTIVE
  The mechanism of spinal cord injury has been thought to be related to the vulnerability of spinal motor neuron cells against ischemia. However, the mechanisms of such vulnerability are not fully understood. Because we previously reported that spinal motor neurons were probably lost as the result of programmed cell death, we investigated a possible mechanism of neuronal death by immunohistochemical analysis for Grp78 and caspase12.
  
  
  METHODS
  We used a rabbit spinal cord ischemia model with a balloon catheter. The spinal cord was removed at 8 hours or 1, 2, or 7 days after 15 minutes of transient ischemia. Histologic changes were studied with hematoxylin-eosin staining. Western blot analysis for Grp78 and caspase12, temporal profiles of Grp78 and caspase12 immunoreactivity, and double-label fluorescence immunocytochemical studies were performed.
  
  
  RESULTS
  The majority of motor neurons were preserved for 2 days but were selectively lost at 7 days of reperfusion. Western blot analysis revealed scarce immunoreactivity for Grp78 and caspase12 in the sham-operated spinal cords. However, immunoreactivity for Grp78 and caspase12 became apparent at 8 hours after transient ischemia, which returned to the baseline level at 1 day. Double-label fluorescence immunocytochemical study revealed that both Grp78 and caspase12 were positive at 8 hours of reperfusion in the same motor neurons that eventually die.
  
  
  CONCLUSIONS
  This study demonstrated that immunoreactivities for both Grp78 and caspase12 were induced in the same motor neuron that eventually dies. These results suggest that endoplasmic reticulum stress was induced in motor neurons by transient spinal cord ischemia in rabbits.
authors.affiliation: Department of Cardiovascular Surgery, National Hospital Organization Sendai Medical Center, Sendai, Japan. sakuraim@mail.tains.tohoku.ac.jp
authors.forename: Masahiro
authors.initials: M
authors.lastname: Sakurai
authors.forename: Goro
authors.initials: G
authors.lastname: Takahashi
authors.forename: Koji
authors.initials: K
authors.lastname: Abe
authors.forename: Takashi
authors.initials: T
authors.lastname: Horinouchi
authors.forename: Yasuto
authors.initials: Y
authors.lastname: Itoyama
authors.forename: Koichi
authors.initials: K
authors.lastname: Tabayashi
mesh_terms: D000818:Animals; D017209:Apoptosis; D053454:Caspase 12; D020169:Caspases / Q000378:metabolism; D004721:Endoplasmic Reticulum / Q000378:metabolism / Q000502:physiology*; D000091342:Endoplasmic Reticulum Chaperone BiP; D006360:Heat-Shock Proteins / Q000378:metabolism; D007150:Immunohistochemistry; D018832:Molecular Chaperones / Q000378:metabolism; D009046:Motor Neurons / Q000378:metabolism* / Q000473:pathology; D011817:Rabbits; D013116:Spinal Cord / Q000166:cytology / Q000378:metabolism; D020760:Spinal Cord Ischemia / Q000378:metabolism / Q000503:physiopathology*
chemical_list: D000091342:Endoplasmic Reticulum Chaperone BiP; D006360:Heat-Shock Proteins; D018832:Molecular Chaperones; D053454:Caspase 12; D020169:Caspases