p25/CDK5 is partially involved in neuronal injury induced by radiofrequency electromagnetic field exposure

Abstract

Purpose: 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.

Materials and 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.