title: Gene expression profile of type II spinal cord decompression sickness.
abstract: METHODS
  This study was an experimental, controlled, animal study.
  
  
  OBJECTIVE
  This study was to determine the changes of molecular pathology in spinal cord decompression sickness (SC-DCS) based on a rabbit model of SC-DCS with the aid of an all-gene expression profile chip.
  
  
  METHODS
  Qingdao, Shandong Province, China.
  
  
  METHODS
  A gene expression profile chip containing 43 803 genes was used to compare the gene expressions in the spinal cords of four male New Zealand white rabbits in the SC-DCS and control groups, respectively. Selected differentially expressed genes were identified with quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) and immunohistochemistry.
  
  
  RESULTS
  The chip hybridization results showed that the SC-DCS group had nine upregulated and seventeen downregulated genes, compared with the control group. These genes were mainly related to inflammation, ion channels, the cell cycle, material transfer and apoptosis. The qRT-PCR results showed that parathyroid hormone and tumor necrosis factor alpha (TNF-α) genes were upregulated compared with the control group (P<0.01). However, the acyl-CoA synthetase and voltage-gated channel genes were downregulated (P<0.05). The immunohistochemical staining results confirmed that there were significantly greater expression levels of TNF-α in the spinal cord tissues of the SC-DCS group compared with the control group.
  
  
  CONCLUSIONS
  The spinal cord lesions of SC-DCS involve multiple gene changes in the rabbit; however, the significance of these findings needs further research. Meanwhile, the gene expression profile chip results provide us with a better understanding of the pathogenesis of DCS.
authors.affiliation: Department of Pathology, General Hospital of Jinan Military Command, Jinan, China.
authors.forename: X
authors.initials: X
authors.lastname: Liu
authors.affiliation: Department of Pathology, General Hospital of Jinan Military Command, Jinan, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Cao
authors.affiliation: Department of Hyperbaric Medicine, No. 401, Hospital of PLA, Qingdao, China.
authors.forename: G
authors.initials: G
authors.lastname: Gao
authors.affiliation: Department of Pathology, General Hospital of Jinan Military Command, Jinan, China.
authors.forename: R
authors.initials: R
authors.lastname: Mao
authors.affiliation: Department of Pathology, General Hospital of Jinan Military Command, Jinan, China.
authors.forename: L
authors.initials: L
authors.lastname: Bi
authors.affiliation: Department of Pathology, General Hospital of Jinan Military Command, Jinan, China.
authors.forename: M
authors.initials: M
authors.lastname: Geng
mesh_terms: D000818:Animals; D003066:Coenzyme A Ligases / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D018450:Disease Progression; D005786:Gene Expression Regulation / Q000502:physiology*; D007473:Ion Channels / Q000235:genetics / Q000378:metabolism; D008297:Male; D020411:Oligonucleotide Array Sequence Analysis / Q000379:methods; D010281:Parathyroid Hormone / Q000235:genetics / Q000378:metabolism; D011817:Rabbits; D013117:Spinal Cord Compression / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D059467:Transcriptome; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism*; D014855:Wallerian Degeneration / Q000209:etiology
chemical_list: D007473:Ion Channels; D010281:Parathyroid Hormone; D014409:Tumor Necrosis Factor-alpha; D003066:Coenzyme A Ligases