{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhao L"],"funding":["Natural Science Foundation of Hebei Province"],"pagination":["477-486"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8921044"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["44(4)"],"pubmed_abstract":["<h4>Background</h4>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.<h4>Objective</h4>This study was designed to investigate the role of miR-200c-3p in regulating inflammatory responses of LPS-treated BV2 cells.<h4>Methods</h4>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.<h4>Results</h4>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.<h4>Conclusions</h4>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."],"journal":["Genes & genomics"],"pubmed_title":["MiR-200c-3p inhibits LPS-induced M1 polarization of BV2 cells by targeting RIP2."],"pmcid":["PMC8921044"],"funding_grant_id":["H2020206322"],"pubmed_authors":["Liu X","Wu J","Yang J","Zhao L","Li C","Hu Y","Xu D","Wang X"],"additional_accession":[]},"is_claimable":false,"name":"MiR-200c-3p inhibits LPS-induced M1 polarization of BV2 cells by targeting RIP2.","description":"<h4>Background</h4>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.<h4>Objective</h4>This study was designed to investigate the role of miR-200c-3p in regulating inflammatory responses of LPS-treated BV2 cells.<h4>Methods</h4>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.<h4>Results</h4>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.<h4>Conclusions</h4>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.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Apr","modification":"2026-03-31T10:59:06.751Z","creation":"2025-04-19T12:59:08.425Z"},"accession":"S-EPMC8921044","cross_references":{"pubmed":["35013887"],"doi":["10.1007/s13258-021-01210-z"]}}