FIG 8.

miR-451a-regulated 14-3-3ζ influences JNK phosphorylation upon infection by JEV/WNV, promoting neuronal apoptosis. Abundance of 14-3-3ζ, p-JNK, total-JNK, total-caspase-9, cleaved-caspase-9, and cleaved-caspase-3 was assessed upon immunoblotting analysis utilizing protein harvested from Neuro-2A-cells infected by JEV (A) or WNV (B) at MOI 3 for 48 h upon transfection with miR-451a inhibitor/inhibitor-control along with 14-3-3ζ-specific esiRNA/Scrambled-(Scr) esiRNA. The immunoblots represent data from three independent experiments with similar outcomes. ß-actin was used as a loading-control. Molecular weight of each probed molecules is stated in kDa beside the corresponding immunoblots. Densitometric analysis of immunoblots indicating effect of 14-3-3ζ esiRNA transfection in the context of miR-451a inhibition and JEV (A, right: ratio of 14-3-3ζ to ß-actin, ratio of phospho-JNK to total-JNK, ratio of cleaved-caspase-9 to total-caspase-9, and ratio of cleaved-caspase-3 to ß-actin) or WNV (B, right: ratio of 14-3-3ζ to ß-actin, ratio of phospho-JNK to total-JNK, ratio of cleaved-caspase-9 to total-caspase-9, and ratio of cleaved-caspase-3 to ß-actin) infection of Neuro-2A cells upon p-JNK (normalized with respect to total-JNK), cleaved-caspase-9 (normalized with respect to total-caspase-9),14-3-3ζ, cleaved-caspase-3 (normalized with respect to ß-actin). Data presented in bar graphs in the form of mean ± SD have been collected from three independent experiments with similar results. **, P < 0.001; *, P < 0.05; ns=non-significant by two-tailed Student's t test.