Open AccessUpregulation of microRNA-206 enhances lipopolysaccharide-induced inflammation and release of amyloid-β by targeting insulin-like growth factor 1 in microglia
Author(s) -
Hongxia Xing,
Shuangxi Guo,
Yi Zhang,
Zhiyong Zheng,
Dan Wang
Publication year - 2016
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2016.5369
Subject(s) - microglia , inflammation , downregulation and upregulation , neuroprotection , insulin like growth factor , lipopolysaccharide , growth factor , trem2 , microrna , cancer research , neuroinflammation , biology , microbiology and biotechnology , immunology , chemistry , pharmacology , receptor , biochemistry , gene
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.