Upregulation of microRNA-206 enhances lipopolysaccharide-induced inflammation and release of amyloid-β by targeting insulin-like growth factor 1 in microglia

Abstract

Activated microglia are capable of facilitating amyloid-β (Aβ) accumulation via the release of inflammatory factors, thus resulting in the exacerbation of Alzheimer's disease (AD). MicroRNAs (miRs) participate in the activation of microglia, which is associated with AD. Insulin-like growth factor 1 (IGF1) is a neuroprotective, anti-inflammatory factor, which is able to accelerate clearance of Aβ peptides. The present study aimed to investigate the precise role of miR-206 and IGF1 in lipopolysaccharide (LPS)-induced microglial inflammation. The expression levels of miR-206 and IGF1 were detected in 60 peripheral blood samples from patients with AD and matched age subjects using quantitative polymerase chain reaction. A dual luciferase reporter gene assay was used to indicate the relationship between miR-206 and IGF1. In addition, the role of miR-206 was determined by gain and loss of function experiments in LPS-treated microglia. The results demonstrated that miR-206 upregulation enhanced LPS-induced inflammation and Aβ release in microglia by directly targeting the 3'-untranslated region of IGF1. These effects were attenuated following treatment with exogenous IGF1, thus indicating that the miR-206/IGF1 signaling pathway may be considered a novel therapeutic target for the treatment of AD-associated microglial inflammation.