title: p25/CDK5 is partially involved in neuronal injury induced by radiofrequency electromagnetic field exposure.
abstract: OBJECTIVE
  Several studies suggest that radiofrequency electromagnetic field (RF-EMF) exposure can induce neuronal injury. The aim of the present work was to investigate whether the cyclin-dependent kinase 5 (CDK5) pathway is involved in neuronal injury induced by RF-EMF exposure.
  
  
  METHODS
  Newborn Sprague-Dawley rats' primary cultured cortical neurons were exposed to pulsed 2.45 GHz RF-EMF for 10 min. The cellular viability was assessed using the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The apoptosis was assessed by Hoechst 33342 and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling co-staining. The protein expressions of CDK5, p35, p25, and phosphorylated tau at Ser(404) were examined by Western blot analysis. The CDK5 activity was detected using a histone-H1 kinase assay.
  
  
  RESULTS
  The cellular viability of neurons was significantly decreased (p < 0.01, Partial Eta Squared [ηp(2)]: 0.554), and the percentage of apoptotic nuclei (p < 0.01, ηp(2) = 0.689), activity of CDK5 (p < 0.05, ηp(2) = 0.589), ratio of p25 and p35 (p < 0.05, ηp(2 =) 0.670), levels of tau phosphorylation at Ser(404) (p < 0.01, ηp(2) = 0.896) were significantly increased after RF-EMF exposure. No significant change was detected in CDK5 expression after RF-EMF exposure. Pretreatment with Roscovitine (a CDK5 inhibitor) significantly blocked the RF-EMF-induced decrease of cellular viability (p < 0.05, ηp(2) = 0.398) and tau hyperphosphorylation at Ser(404) (p < 0.01, ηp(2 =) 0.917), but did not significantly block the RF-EMF-induced apoptosis (p > 0.05, ηp(2) = 0.130).
  
  
  CONCLUSIONS
  These results suggest that abnormal activity of p25/CDK5 is partially involved in primary cultured cortical neuron injury induced by RF-EMF exposure.
authors.affiliation: Key Laboratory of Medical Protection for Electromagnetic Radiation, Ministry of Education, Third Military Medical University , Chongqing, 400038 , P. R. China.
authors.forename: Yanwen
authors.initials: Y
authors.lastname: Zhang
authors.forename: Fei
authors.initials: F
authors.lastname: She
authors.forename: Li
authors.initials: L
authors.lastname: Li
authors.forename: Chunhai
authors.initials: C
authors.lastname: Chen
authors.forename: Shangcheng
authors.initials: S
authors.lastname: Xu
authors.forename: Xue
authors.initials: X
authors.lastname: Luo
authors.forename: Min
authors.initials: M
authors.lastname: Li
authors.forename: Mindi
authors.initials: M
authors.lastname: He
authors.forename: Zhengping
authors.initials: Z
authors.lastname: Yu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000528:radiation effects; D002470:Cell Survival / Q000187:drug effects / Q000528:radiation effects; D051360:Cyclin-Dependent Kinase 5 / Q000037:antagonists & inhibitors / Q000378:metabolism*; D004574:Electromagnetic Fields / Q000009:adverse effects*; D004789:Enzyme Activation / Q000187:drug effects / Q000528:radiation effects; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects / Q000528:radiation effects; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000201:enzymology / Q000528:radiation effects*; D010766:Phosphorylation / Q000187:drug effects / Q000528:radiation effects; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D011846:Radio Waves / Q000009:adverse effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D016875:tau Proteins / Q000378:metabolism
chemical_list: D047428:Protein Kinase Inhibitors; D016875:tau Proteins; D051360:Cyclin-Dependent Kinase 5