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. 2015 Jan 28;9:3. doi: 10.3389/fncel.2015.00003

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Copyright © 2015 Uribe, Kawas, Harding and Coffin.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Dihexa-mediated protection is inhibited by MEK, Akt, and TOR inhibitors. (A) Co-treatment with 1 μM MEK or Akt inhibitors (UO126 and Akt Inhibitor VIII, respectively) partially attenuates Dihexa-dependent protection (Two-way ANOVA; Dihexa: F_(3,144) = 37.13 p < 0.001). When comparing the 1 μM Dihexa treatment vs. 1 μM Dihexa plus 1 μM UO126 p-values are as follows: 50 μM neomycin (p < 0.05), 100 μM neomycin (p < 0.05), 200 μM neomycin (p < 0.001), and 400 μM neomycin (p < 0.05). When comparing the 1 μM Dihexa treatment vs. 1 μM Dihexa plus 1 μM Akt inhibitor VIII p-values are as follows: 50 μM neomycin (p > 0.05), 100 μM neomycin (p < 0.05), 200 μM neomycin (p < 0.001), 400 μM neomycin (p > 0.05). (B) Co-treatment with 10 μM of the TOR inhibitor, rapamycin, also partially attenuates Dihexa-mediated protection from neomycin (Two-way ANOVA; Dihexa: F_(3,120) = 70.41 p < 0.001). When comparing the 1 μM Dihexa treatment vs. 1 μM Dihexa plus 10 μM rapamycin p-values were as follows: 50 μM neomycin (p < 0.001), 100 μM neomycin (p < 0.001), 200 and 400 μM neomycin (p > 0.05). N = 6–9 animals per treatment, error bars represent ± s.e.m.