title: Effects of ApoE on intracellular calcium levels and apoptosis of neurons after mechanical injury.
abstract: OBJECTIVE
  The current study aimed to explore the effects of apolipoprotein e (ApoE) on intracellular calcium ([Ca(2+)]i) and apoptosis of neurons after mechanical injury in vitro.
  
  
  METHODS
  A neuron mechanical injury model was established after primary neurons obtained from APOE knockout and wild-type (WT) mice, and four experimental groups were generated: Group-ApoE4, Group-ApoE3, Group-ApoE(-) and Group-WT. Recombinant ApoE4 and ApoE3 were added to Group-ApoE4 and Group-ApoE3 respectively, and Group-ApoE(-) and Group-WT were control groups. Intracellular calcium was labeled by fluo-3/AM and examined using laser scanning confocal microscope and flow cytometry, and the apoptosis of neurons was also evaluated.
  
  
  RESULTS
  The intracellular calcium levels and apoptosis rates of mice neurons were significantly higher in Group-ApoE4 than in Group-ApoE3 and Group-WT after mechanical injury. However, without mechanical injury on neurons, no significant differences in intracellular calcium levels and apoptosis rates were found among all four experimental groups. The effects of ApoE4 on intracellular calcium levels and apoptosis rates of injured neurons were partly decreased by EGTA treatment.
  
  
  CONCLUSIONS
  Compared with ApoE3-treatment and WT neurons, ApoE4 caused higher intracellular calcium levels and apoptosis rates of neurons after mechanical injury. This suggested APOE polymorphisms may affect neuron apoptosis after mechanical injury through different influences on intracellular calcium levels.
authors.affiliation: Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, PR China.
authors.forename: L
authors.initials: L
authors.lastname: Jiang
authors.affiliation: Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, PR China.
authors.forename: J
authors.initials: J
authors.lastname: Zhong
authors.affiliation: Chongqing Medical University, PR China.
authors.forename: X
authors.initials: X
authors.lastname: Dou
authors.affiliation: Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, PR China.
authors.forename: C
authors.initials: C
authors.lastname: Cheng
authors.affiliation: Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, PR China.
authors.forename: Z
authors.initials: Z
authors.lastname: Huang
authors.affiliation: Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, PR China. Electronic address: sunxch1445@qq.com.
authors.forename: X
authors.initials: X
authors.lastname: Sun
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D053318:Apolipoprotein E3 / Q000494:pharmacology; D053327:Apolipoprotein E4 / Q000494:pharmacology; D001057:Apolipoproteins E / Q000172:deficiency / Q000502:physiology*; D017209:Apoptosis / Q000187:drug effects / Q000235:genetics*; D002118:Calcium / Q000378:metabolism*; D002540:Cerebral Cortex / Q000166:cytology; D005434:Flow Cytometry; D005786:Gene Expression Regulation; D007424:Intracellular Fluid / Q000378:metabolism*; D051379:Mice; D018345:Mice, Knockout; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D010812:Physical Stimulation / Q000009:adverse effects*; D013314:Stress, Mechanical; D013997:Time Factors
chemical_list: D053318:Apolipoprotein E3; D053327:Apolipoprotein E4; D001057:Apolipoproteins E; D002118:Calcium
keywords: APOE polymorphism; TBI; intracellular calcium level; mechanical injury; neuron