title: Endoplasmic reticulum stress response in the rat contusive spinal cord injury model-susceptibility in specific cell types.
abstract: METHODS
  Focus group study.
  
  
  OBJECTIVE
  To investigate cell-specific endoplasmic reticulum (ER) stress reactions in contusive spinal cord by evaluating the expression of the glucose-regulated protein 78 (GRP78) and C/EBP homologous transcription factor protein (CHOP) using immunohistochemical staining.
  
  
  METHODS
  Data were analysed at Tokai University School of Medicine in Japan.
  
  
  METHODS
  The authors generated rat spinal cord injury (SCI) models using an IH-Impactor (100 kdyne(LI), 200 kdyne (HI)). Rats were killed at 1, 3, 5, 7 and 14 days post operation (dpo). Spinal cord sections were prepared and the expression ratio of GRP78 and CHOP was evaluated in oligodendrocyte precursor cells (OPCs) (NG2+), oligodendrocytes (OLs) (APC+), neurons (NeuN+) and astrocytes (GFAP+) using double immunohistochemical staining. We examined an area 8 mm distal from SCI-epicenter.
  
  
  RESULTS
  Compared with the sham group, both injured groups had higher GRP78 expression ratio in contused spinal cord at 1 dpo. GRP78 expression ratio was highest in GFAP+ cells of both groups, and lowest in NG2+ cells. Although GRP78 was expressed strongly immediately after SCI in the both groups, increased CHOP expression was observed only in the HI group. The CHOP expression in NG2+ cells was significantly higher than that observed in GFAP+ cells at 5 dpo.
  
  
  CONCLUSIONS
  Although the ER stress response contributes to cell survival in the low-stress SCI conditions, the ER stress response induces an apoptotic cascade in high-stress SCI conditions. The ER response varies according to cell type, with the highest observed in astrocytes, and the lowest observed in oligodendrocyte precursor cells.
authors.affiliation: Department of Orthopaedic Surgery, Surgical Science, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
authors.forename: D
authors.initials: D
authors.lastname: Matsuyama
authors.affiliation: Department of Orthopaedic Surgery, Surgical Science, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Watanabe
authors.affiliation: Department of Orthopaedic Surgery, Surgical Science, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Suyama
authors.affiliation: Department of Orthopaedic Surgery, Surgical Science, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Kuroiwa
authors.affiliation: Department of Orthopaedic Surgery, Surgical Science, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
authors.forename: J
authors.initials: J
authors.lastname: Mochida
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000378:metabolism; D004195:Disease Models, Animal; D059865:Endoplasmic Reticulum Stress / Q000502:physiology*; D006360:Heat-Shock Proteins / Q000032:analysis* / Q000096:biosynthesis; D007150:Immunohistochemistry; D008297:Male; D009474:Neurons / Q000378:metabolism; D009836:Oligodendroglia / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013119:Spinal Cord Injuries / Q000378:metabolism* / Q000473:pathology; D013234:Stem Cells / Q000378:metabolism; D051742:Transcription Factor CHOP / Q000032:analysis* / Q000096:biosynthesis; D000091342:Endoplasmic Reticulum Chaperone BiP
chemical_list: D006360:Heat-Shock Proteins; D051742:Transcription Factor CHOP; C497251:Ddit3 protein, rat; C051684:GRP78 protein, rat; D000091342:Endoplasmic Reticulum Chaperone BiP