title: Autophagy is activated and might protect neurons from degeneration after traumatic brain injury.
abstract: OBJECTIVE
  To investigate changes of autophagy after traumatic brain injury (TBI) and its possible role.
  
  
  METHODS
  Rat TBI model was established by controlled cortical injury system. Autophagic double membrane structure was detected by transmission electronic microscope. Microtubule-associated protein 1 light chain 3 (LC3) and Beclin 1 were also used to investigate the activation of autophagy post-TBI. Double labeling with LC3 and caspase-3, or Beclin 1 and Fluoro-Jade to show the relationship between autophagy and apoptosis or neuron degeneration after TBI.
  
  
  RESULTS
  An increase of autophagic double membrane structure was observed in early stage (1 h), and the increase lasted for at least 32 d post-TBI. LC3 and Beclin 1 proteins also began to elevate at 1 h time point post-TBI in neurons, 3 d later in astrocytes, and peaked at about 8 d post-TBI. In both cell types, LC3 and Beclin 1 maintained at a high level until 32 d post-TBI. Most LC3 and Beclin 1 positive cells were near the side (including hippocampus), but not in the core of the injury. In addition, in the periphery of the injury site, not all caspase-3 positive (+) cells merged with LC3 (+) cells post-TBI; In hippocampal area, almost all Beclin 1 (+) neurons did not merge with Fluoro-Jade (+) neurons from 1 h to 48 h post-TBI.
  
  
  CONCLUSIONS
  Autophagy is activated and might protect neurons from degeneration at early stage post-TBI and play a continuous role afterwards in eliminating aberrant cell components.
authors.affiliation: Institute of Forensic Medicine, Laboratory of Aging and Nerves Diseases, Soochow University, Suzhou, China.
authors.forename: Yan-Bo
authors.initials: YB
authors.lastname: Zhang
authors.forename: Sheng-Xing
authors.initials: SX
authors.lastname: Li
authors.forename: Xi-Ping
authors.initials: XP
authors.lastname: Chen
authors.forename: Li
authors.initials: L
authors.lastname: Yang
authors.forename: Yun-Ge
authors.initials: YG
authors.lastname: Zhang
authors.forename: Ran
authors.initials: R
authors.lastname: Liu
authors.forename: Lu-Yang
authors.initials: LY
authors.lastname: Tao
mesh_terms: D000818:Animals; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism*; D001253:Astrocytes / Q000378:metabolism / Q000473:pathology; D001343:Autophagy; D000071186:Beclin-1; D001921:Brain / Q000378:metabolism* / Q000473:pathology; D001930:Brain Injuries / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D053148:Caspase 3 / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism / Q000473:pathology; D019610:Cytoprotection; D004195:Disease Models, Animal; D005452:Fluoresceins; D005455:Fluorescent Antibody Technique; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008297:Male; D046529:Microscopy, Electron, Transmission; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D009410:Nerve Degeneration / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D009930:Organic Chemicals; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D015854:Up-Regulation
chemical_list: D051017:Apoptosis Regulatory Proteins; D000071186:Beclin-1; D053148:Caspase 3; D005452:Fluoresceins; D008869:Microtubule-Associated Proteins; D009930:Organic Chemicals; C512829:Becn1 protein, rat; C526109:Anxa3 protein, rat; C435731:fluoro jade