title: Enhancement of heat shock protein expression after transient ischemia in the preconditioned spinal cord of rabbits.
abstract: OBJECTIVE
  This investigation was designed to evaluate the mechanism used to acquire a tolerance to spinal ischemia. We investigated inductions of the heat shock protein (HSP) 70 gene and protein in rabbit spinal cord with or without preconditioning.
  
  
  METHODS
  Neurologic function, morphologic changes, and inductions of HSP70 messenger RNA (mRNA) and protein were compared in the cases of a 15-minute ischemia 2 days after sham treatment and a 15-minute ischemia 2 days after 10-minute preconditioning.
  
  
  RESULTS
  HSP70 mRNA was induced at 8 hours of reperfusion after a 15-minute ischemia 2 days after sham treatment. HSP70 protein was induced slightly in selective motor neuron cells at 8 hours of reperfusion, and about 70% of motor neuron cells showed selective cell death after 7 days of reperfusion (p < 0.01). On the other hand, large populations of the motor neuron cells survived at 7 days after the 15-minute ischemia that was applied at 2 days after preconditioning (p < 0.01). HSP70 mRNA was induced persistently as compared with the case of a 15-minute ischemia 2 days after sham treatment. The motor neuron cells strongly produced immunoreactive HSP70 from 8 hours to 2 days.
  
  
  CONCLUSIONS
  Preconditioning with 10-minute ischemia enhanced and prolonged the HSP70 gene expression at both mRNA and protein levels and saved the motor neuron cells from subsequent lethal ischemia. These changes of HSP70 gene expression may play an important role in the acquisition of ischemic tolerance of motor neuron cells in rabbit spinal cord.
authors.affiliation: Department of Thoracic and Cardiovascular Surgery, Tohoku University School of Medicine, Sendai, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Sakurai
authors.forename: T
authors.initials: T
authors.lastname: Hayashi
authors.forename: K
authors.initials: K
authors.lastname: Abe
authors.forename: M
authors.initials: M
authors.lastname: Aoki
authors.forename: M
authors.initials: M
authors.lastname: Sadahiro
authors.forename: K
authors.initials: K
authors.lastname: Tabayashi
mesh_terms: D000818:Animals; D001012:Aorta, Abdominal / Q000503:physiopathology; D001259:Ataxia / Q000209:etiology / Q000503:physiopathology; D015152:Blotting, Northern; D002404:Catheterization; D002452:Cell Count; D016923:Cell Death; D002470:Cell Survival; D005069:Evaluation Studies as Topic; D005786:Gene Expression Regulation; D018840:HSP70 Heat-Shock Proteins / Q000032:analysis / Q000235:genetics / Q000378:metabolism*; D006614:Hindlimb / Q000502:physiology; D007150:Immunohistochemistry; D007511:Ischemia / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D019194:Ischemic Preconditioning; D009046:Motor Neurons / Q000378:metabolism / Q000473:pathology; D009460:Neurologic Examination; D010264:Paraplegia / Q000209:etiology / Q000503:physiopathology; D010291:Paresis / Q000209:etiology / Q000503:physiopathology; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics; D011817:Rabbits; D012039:Regional Blood Flow; D015424:Reperfusion; D013116:Spinal Cord / Q000098:blood supply* / Q000473:pathology / Q000503:physiopathology; D013997:Time Factors
chemical_list: D018840:HSP70 Heat-Shock Proteins; D012333:RNA, Messenger