Inflammation is the body's normal self-protection mechanism to eliminate pathogens and resist pathogen invasion. The excessive inflammatory response may lead to inflammatory lesions. The mechanisms accounting for inflammation remain hazy. MicroRNAs (miRNAs) have been proposed to have crucial effects on inflammation. In the current study, we reported that lipopolysaccharide (LPS) stimulation increases the expression levels of inflammatory cytokines and the cell cycle progression was suppressed in RAW264.7 cells. Meanwhile, the expression of miR-322 was significantly downregulated after LPS treated. Bioinformatics predictions revealed a potential binding site of miR-322 in 3′-untranslated region (3′-UTR) of NF-κB1 (P50) and it was further confirmed by luciferase assay. Moreover, both the mRNA and protein levels of NF-κB1 (P50) were downregulated by miR-322 in RAW264.7. Subsequently, we demonstrate that miR-322 mimics decrease the expression levels of inflammatory cytokines and cell cycle repression can be rescued following LPS treated in RAW264.7 cells. The anti-inflammatory cytokines expression including IL-4 and IL-10 were significant up-regulation. Furthermore, miR-322 also could promote RAW264.7 cells proliferation. These results demonstrate that miR-322 is a negative regulator of inflammatory response by targeting NF-κB1 (P50).
- NF-κB1 (P50)
- ©2016 The Author(s)
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