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KMID : 0381120220440040477
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Genes and Genomics
2022 Volume.44 No. 4 p.477 ~ p.486
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MiR-200c-3p inhibits LPS-induced M1 polarization of BV2 cells by targeting RIP2
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Zhao Lei
Liu Xiaosong
Yang Jiankai
Wang Xiaoliang
Liu Xiaomeng
Wu Jianliang
Li Chen
Xu Donggang
Hu Yuhua
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Abstract
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Background: Microglia are important immune cells, which can be induced by lipopolysaccharide (LPS) into M1 phenotype that express pro-inflammatory cytokines. Some studies have shown that microRNAs play critical roles in microglial activation.
Objective: This study was designed to investigate the role of miR-200c-3p in regulating inflammatory responses of LPS-treated BV2 cells.
Methods: The expression of miR-200c-3p in BV2 cells was detected by real-time PCR. Receptor-interacting protein 2 (RIP2) was predicted as a target gene of miR-200c-3p. Their relationship was verified by dual-luciferase reporter assay. The function of miR-200c-3p and RIP2 in microglial polarization and NF-κB signaling was further evaluated.
Results: LPS treatment reduced miR-200c-3p expression in a dose-dependent and time-dependent manner in BV2 cells. LPS treatment increased the expression of M1 phenotype markers inducible nitric oxide synthase (iNOS) and major histocompatibility complex class (MHC)-II, promoted the release of pro-inflammatory cytokines interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α, and enhanced the nuclear translocation and phosphorylation of nuclear factor-kappaB (NF-κB) p65. Reversely, miR-200c-3p mimics down-regulated the levels of these inflammatory factors. Furthermore, RIP2 was identified to be a direct target of miR-200c-3p. RIP2 knockdown had a similar effect to miR-200c-3p mimics. Overexpression of RIP2 eliminated the inhibitory effect of miR-200c-3p on LPS-induced M1 polarization and NF-κB activation in BV2 cells.
Conclusions: MiR-200c-3p mimics suppressed LPS-induced microglial M1 polarization and NF-κB activation by targeting RIP2. MiR-200c-3p/RIP2 might be a potential therapeutic target for the treatment of neuroinflammation-associated diseases.
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KEYWORD
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LPS treatment, miR-200c-3p, RIP2, Microglia activation
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