MicroRNA-155 contributes to the occurrence of epilepsy through the PI3K/Akt/mTOR signaling pathway

Abstract

Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to measure the expression of microRNA-155 in patients with temporal lobe epilepsy. Commercial kit and western blot analysis were used to measure gap-associated protein expression. The aim of the present study was to investigate the effect of microRNA-155 (miRNA-155) in the occurrence of epilepsy and the molecular mechanism involved. In patients with temporal lobe epilepsy, miRNA-155 expression was evidently higher than that in patients of the normal volunteers group. Overexpression of miRNA-155 resulted in decreased brain-derived neurotrophic factor (BDNF) and tropomyosin receptor kinase B (TrkB) protein expression, increased caspase-3 activity, tumor protein p53 (p53) and apoptosis regulator BAX (Bax) protein expression, and inhibited phosphoinositide 3-kinase (PI3K), phosphorylated (p-)protein kinase B (Akt) and p-mechanistic target of rapamycin (mTOR) protein expression in epilepsy cells. PI3K inhibitor accelerated the effect of miRNA-155 on the inhibition of BDNF and TrkB protein expression, the promotion of caspase-3 activity, p53 and Bax protein expression, and the inhibition of PI3K, p-Akt and p-mTOR protein expression in epilepsy cells. The present findings indicate that miRNA-155 contributes to the occurrence of epilepsy through the PI3K/Akt/mTOR signaling pathway.