miR-26b inhibits total neurite outgrowth, promotes cells apoptosis and downregulates neprilysin in Alzheimer’s disease

This study aimed to investigate the effect of miR-26b expression on neurites outgrowth and cells apoptosis in PC12 cellular model of Alzheimer’s disease (AD). PC12 cells were stimulated by nerve growth factor and insulted by Aβ1-42 to establish PC12 cellular AD model. Methyl thiazolyl tetrazolium (MTT) assay was then used to detect cells viability. Blank mimic, miR-26b mimic, blank inhibitor and miR-26b inhibitor plasmids were transferred into PC12 cellular AD models as NC1-mimic, miR-26b mimic, NC2-inhibitor and miR-26b inhibitor groups respectively. mRNA level, protein level, total neurite outgrowth and cells apoptosis were determined by qPCR, western blot, microscope and Hoechst/PI, respectively. MTT reduction rate was decreased in Aβ1-42 insult group compared to control group (P<0.001). After plasmids transfection, the total neuritis growth was found to be reduced in miR-26b mimic group compared with NC1-mimic group (P<0.05) while was elevated in miR-26b inhibitor group compared with NC2-inhibitor group (P<0.01). As to cells apoptosis, the percentage of apoptosis cells was increased in miR-26b mimic group than NC1-mimic group (P<0.05), and was decreased in miR-26b inhibitor group than NC2-inhibitor group (P<0.05). In addition, neprilysin (NEP) protein and mRNA expressions were decreased in miR-26b mimic group than NC1-mimic group and was increased in miR-26b inhibitor group than NC2-inhibitor group. However, protein or mRNA expression of EIF2S1 and αTTP was not affected by miR-26b. In conclusion, miR-26b inhibits neurite outgrowth, induces cells apoptosis and downregulates NEP expression in PC12 cellular AD model.