MicroRNA-20b-5p aggravates neuronal apoptosis induced by β-Amyloid via down-regulation of Ras homolog family member C in Alzheimer's disease.

Recent studies have reported that microRNAs are abnormally expressed in brain tissues of Alzheimers disease (AD) patients. However, the accurate function of miR-20b-5p in AD has not been elucidated. We intended to investigate the role and underlying mechanism of miR-20b-5p in AD. The expression of miR-20b-5p was increased, and the expression of RhoC was decreased in the hippocampus of Appswe/PS△E 9 mice. In order to construct a cell model in vitro to study the underlying action mechanism, PC12 cells were treated with Aβ25-35. The cell apoptosis detected by flow cytometry and the expression of cleaved-caspase-3 detected by western blot were both remarkably increased in PC12 cells treated with Aβ25-35, but they were reduced by miR-20b-5p inhibitor. In addition, MTT test showed that the cell survival rate in Aβ25-35 + miR-20b-5p inhibitor group was higher than that in Aβ25-35 + NC inhibitor group. Double luciferase reporter gene analysis confirmed that the binding site of miR-20b-5p was in 3'- UTR of RhoC mRNA. Knockdown of RhoC increased neuronal apoptosis induced by Aβ25-35 and the expression of cleaved-caspase-3, while miR-20b-5p inhibitor reversed these effects. Knockdown of RhoC aggravated the inhibition effect on cell viability induced by Aβ25-35, while miR-20b-5p inhibitor diminished these effects. In conclusion, inhibition of miR-20b-5p attenuates apoptosis induced by Aβ25-35 in PC12 cells through targeting RhoC. Therefore, miR-20b-5p may be a perspective curative target for AD.