Long Noncoding RNA SNHG1 Promotes Lipopolysaccharide-Induced Activation and Inflammation in Microglia via Targeting miR-181b

Abstract

<b><i>Introduction:</i></b> Long noncoding RNA small nuclear host gene 1 (SNHG1) was involved in neuroinflammation in microglial BV-2 cells; however, its interaction with microRNA (miR)-181b in lipopolysaccharide (LPS)-induced BV-2 cells remained poor. <b><i>Methods:</i></b> BV-2 cells were treated with LPS and then were subjected to observation on morphology and immunofluorescence staining. After transfection, levels of inflammatory cytokines interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) were determined with enzyme-linked immunosorbent assay (ELISA). The potential binding sites between SNHG1 and miR-181b were confirmed using dual-luciferase reporter assay. Quantitative real-time polymerase chain reaction and Western blot were applied for detecting the mRNA and protein expressions of proinflammatory cytokines, ionized calcium-binding adapter molecule 1 (Iba1), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS). <b><i>Results:</i></b> LPS led to the morphological changes and activation of BV-2 cells. The transfection of SNHG1 overexpression vector further promoted LPS-induced SNHG1 upregulation, inflammatory cytokines (IL-1β, IL-6, and TNF-α) generation and Iba-1, COX-2, and iNOS expressions, whereas silencing SNHG1 did the opposite. miR-181b functions as a downstream miRNA of SNHG1. In LPS-treated cells, the inhibition of miR-181b induced by SNHG1 promoted inflammation response and the expressions of Iba-1, COX-2, and iNOS. <b><i>Conclusion:</i></b> SNHG1 was involved in LPS-induced microglial activation and inflammation response via targeting miR-181b, providing another evidence of the roles of SNHG1 implicated in neuroinflammation of microglia.

Small nucleolar RNA host gene 1 silence inhibits the lipopolysaccharide-induced microglial apoptosis and inflammation

“…In recent years, SNHG1's effects on microglia have also been gradually unveiled. For example, Dong J et al [13] reported that SNHG1 accelerated LPSinduced microglial activation and inflammation by targeting miR-181b. Consistently, we found a marked increase of SNHG1 in BV2 under LPS inducement, and enhanced inhibition of cell apoptosis following SNHG1 knockdown.…”

Biology of cyclooxygenase-2: An application in depression therapeutics

“…Natural drug substances can improve the levels of oxidative stress and neuroinflammation in depression, Muhammad et al ( 41 ) used carvacrol to treat rats with depressive-like behavior induced by LPS, and significant neuronal alterations as well as elevated levels of inflammatory cytokines, such as TNF-α, COX-2 and c-Jun N-terminal kinase (p JNK). lPS stimulates microglia activation and inflammatory responses and upregulates mRNA and protein expression of inflammatory mediators such as COX-2 ( 42 , 43 ). These inflammatory mediators can further mediate changes in the intestinal flora and disturbances in their metabolites, affecting brain function and depression.…”

Altered Lnc-EGFR, SNHG1, and LincRNA-Cox2 Profiles in Patients with Relapsing-Remitting Multiple Sclerosis: Impact on Disease Activity and Progression

“…The long noncoding RNA small nucleolar RNA host gene 1 (SNHG1) is another newly identified lncRNA that was found to be upregulated in the brain specimens derived from patients with Parkinson’s disease (PD) [ 28 ] and in MPTP-induced PD mouse models [ 29 ]. Additionally, SNHG1 has been implicated in microglial activation and neuroinflammation [ 29 , 30 ]. Furthermore, SNHG1 overexpression was shown to be correlated with the activation of the NLRP3 inflammasome and enhanced expression of NLRP3, ASC, and cleaved caspase-1 in lipopolysaccharide-stimulated BV2 microglial cells in vitro [ 29 ].…”