title: The role of Fas-mediated apoptosis after traumatic spinal cord injury.
abstract: METHODS
  Functional recovery and histopathological change after spinal cord injury in the Fas-deficient mice and the wild-type mice were investigated.
  
  
  OBJECTIVE
  To investigate the role of the Fas/Fas ligand (FasL) system as a signal transduction pathway leading to apoptosis after spinal cord injury.
  
  
  BACKGROUND
  [corrected] Apoptosis observed after spinal cord injury has recently gained widespread interest as a cause of collateral damage after the initial injury. Apoptosis mediated by the Fas antigen in the postischemic brain or spinal cord was reported. Recently, the upregulation of Fas after spinal cord injury was also reported. However, the influence of Fas-mediated apoptosis on the extent of the secondary spinal cord injury has not yet been clarified.
  
  
  METHODS
  We investigated Fas-mediated apoptosis after spinal cord injury and examined the behavioral changes and the histopathological changes after spinal cord injury using MRL/Mp-lpr/lpr (MRL/lpr) mice, which were Fas-deficient mutant mice, and MRL/Mp-+/+ (MRL/+) mice, which were Fas-positive wild-type mice.
  
  
  RESULTS
  Locomotor recovery after spinal cord injury in MRL/lpr mice was superior to that observed in MRL/+ mice. In addition, the damaged area in MRL/lpr mice was significantly smaller than that seen in MRL/+ mice. Further, the frequency of apoptotic cells in the injured spinal cord of MRL/lpr mice was significantly less than that in MRL/+ mice.
  
  
  CONCLUSIONS
  We demonstrated the appearance of Fas-mediated apoptosis in the spinal cord after spinal cord injury. In addition, we elucidated for the first time that Fas-mediated apoptosis following spinal cord injury played an important role in the spinal cord damage and the ultimate neurologic injury.
authors.affiliation: Department of Orthopaedic Surgery, Toyama Medical and Pharmaceutical University, Toyama, Japan. g7410006@ms.toyama-mpu.ac.jp
authors.forename: Osamu
authors.initials: O
authors.lastname: Yoshino
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Matsuno
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nakamura
authors.forename: Kazuo
authors.initials: K
authors.lastname: Yudoh
authors.forename: Yumiko
authors.initials: Y
authors.lastname: Abe
authors.forename: Takashi
authors.initials: T
authors.lastname: Sawai
authors.forename: Miwa
authors.initials: M
authors.lastname: Uzuki
authors.forename: Shin
authors.initials: S
authors.lastname: Yonehara
authors.forename: Tomoatsu
authors.initials: T
authors.lastname: Kimura
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002921:Cicatrix / Q000473:pathology; D003288:Contusions / Q000378:metabolism / Q000473:pathology; D053222:Fas Ligand Protein; D007124:Immunoenzyme Techniques; D020287:In Situ Nick-End Labeling; D008297:Male; D008562:Membrane Glycoproteins / Q000032:analysis / Q000502:physiology*; D051379:Mice; D019463:Mice, Inbred MRL lpr; D008854:Microscopy, Electron; D010243:Paralysis / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D020127:Recovery of Function; D015398:Signal Transduction; D013116:Spinal Cord / Q000648:ultrastructure; D013119:Spinal Cord Injuries / Q000150:complications / Q000378:metabolism / Q000473:pathology*; D019014:fas Receptor / Q000032:analysis / Q000235:genetics / Q000502:physiology*
chemical_list: D053222:Fas Ligand Protein; C505658:Fasl protein, mouse; D008562:Membrane Glycoproteins; D019014:fas Receptor