MicroRNA-124 mediates the cholinergic anti-inflammatory action through inhibiting the production of pro-inflammatory cytokines
The vagus nerve can control inflammatory response through a ＇cholinergic anti-inflammatory pathway＇, which is mediated by the α7-nicotinic acetylcholine receptor （α7nAChR） on macrophages. However, the intracellular mechanisms that link a7nAChR activation and pro-inflammatory cytokine production rema...
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| Veröffentlicht in: | Cell research 2013-11, Vol.23 (11), p.1270-1283 |
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| creator | Sun, Yang Li, Qi Gui, Huan Xu, Dong-Ping Yang, Yi-Li Su, Ding-Feng Liu, Xia |
| description | The vagus nerve can control inflammatory response through a ＇cholinergic anti-inflammatory pathway＇, which is mediated by the α7-nicotinic acetylcholine receptor （α7nAChR） on macrophages. However, the intracellular mechanisms that link a7nAChR activation and pro-inflammatory cytokine production remain not well understood. In this study, we found that miR-124 is upregulated by cholinergic agonists in LPS-exposed cells and mice. Utilizing miR-124 mimic and siRNA knockdown, we demonstrated that miR-124 is a critical mediator for the cholinergic anti-inflammatory action. Furthermore, our data indicated that miR-124 modulates LPS-induced cytokine production by targeting signal transducer and activator of transcription 3 （STAT3） to decrease IL-6 production and TNF-o converting enzyme （TACE） to reduce TNF-α release. These results also indicate that miR-124 is a potential therapeutic target for the treatment of inflammatory diseases. |
| doi_str_mv | 10.1038/cr.2013.116 |
| format | Article |
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However, the intracellular mechanisms that link a7nAChR activation and pro-inflammatory cytokine production remain not well understood. In this study, we found that miR-124 is upregulated by cholinergic agonists in LPS-exposed cells and mice. Utilizing miR-124 mimic and siRNA knockdown, we demonstrated that miR-124 is a critical mediator for the cholinergic anti-inflammatory action. Furthermore, our data indicated that miR-124 modulates LPS-induced cytokine production by targeting signal transducer and activator of transcription 3 （STAT3） to decrease IL-6 production and TNF-o converting enzyme （TACE） to reduce TNF-α release. These results also indicate that miR-124 is a potential therapeutic target for the treatment of inflammatory diseases.</description><identifier>ISSN: 1001-0602</identifier><identifier>EISSN: 1748-7838</identifier><identifier>DOI: 10.1038/cr.2013.116</identifier><identifier>PMID: 23979021</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/250/127 ; 631/250/2504/342 ; 631/250/256 ; 631/337/384/331 ; Acetylcholine receptors ; ADAM Proteins - metabolism ; ADAM17 Protein ; alpha7 Nicotinic Acetylcholine Receptor - metabolism ; Animals ; Biomedical and Life Sciences ; Cell Biology ; Cells, Cultured ; Cholinergic Neurons - metabolism ; Cytokines - biosynthesis ; Cytokines - genetics ; Cytokines - secretion ; HEK293 Cells ; Humans ; Interleukin-6 - biosynthesis ; Interleukin-6 - genetics ; Life Sciences ; Lipopolysaccharides - antagonists & inhibitors ; Lipopolysaccharides - pharmacology ; Macrophages - metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; MicroRNAs - metabolism ; Original ; original-article ; Sepsis - chemically induced ; Sepsis - genetics ; Sepsis - metabolism ; Sepsis - pathology ; siRNA ; STAT3 ; STAT3 Transcription Factor - metabolism ; TNF-α ; Transcription, Genetic ; Tumor Necrosis Factor-alpha - biosynthesis ; Tumor Necrosis Factor-alpha - genetics ; 乙酰胆碱受体 ; 介导 ; 抗炎作用 ; 细胞因子 ; 胆碱能</subject><ispartof>Cell research, 2013-11, Vol.23 (11), p.1270-1283</ispartof><rights>The Author(s) 2013</rights><rights>Copyright Nature Publishing Group Nov 2013</rights><rights>Copyright © 2013 Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences 2013 Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c571t-a7f7ee45b9c1d220e9f2d311c6e69be1fae086dc5b13a56692d3d2a6e9593a923</citedby><cites>FETCH-LOGICAL-c571t-a7f7ee45b9c1d220e9f2d311c6e69be1fae086dc5b13a56692d3d2a6e9593a923</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/85240X/85240X.jpg</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3817544/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3817544/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,886,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23979021$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sun, Yang</creatorcontrib><creatorcontrib>Li, Qi</creatorcontrib><creatorcontrib>Gui, Huan</creatorcontrib><creatorcontrib>Xu, Dong-Ping</creatorcontrib><creatorcontrib>Yang, Yi-Li</creatorcontrib><creatorcontrib>Su, Ding-Feng</creatorcontrib><creatorcontrib>Liu, Xia</creatorcontrib><title>MicroRNA-124 mediates the cholinergic anti-inflammatory action through inhibiting the production of pro-inflammatory cytokines</title><title>Cell research</title><addtitle>Cell Res</addtitle><addtitle>Cell Research</addtitle><description>The vagus nerve can control inflammatory response through a ＇cholinergic anti-inflammatory pathway＇, which is mediated by the α7-nicotinic acetylcholine receptor （α7nAChR） on macrophages. However, the intracellular mechanisms that link a7nAChR activation and pro-inflammatory cytokine production remain not well understood. In this study, we found that miR-124 is upregulated by cholinergic agonists in LPS-exposed cells and mice. Utilizing miR-124 mimic and siRNA knockdown, we demonstrated that miR-124 is a critical mediator for the cholinergic anti-inflammatory action. Furthermore, our data indicated that miR-124 modulates LPS-induced cytokine production by targeting signal transducer and activator of transcription 3 （STAT3） to decrease IL-6 production and TNF-o converting enzyme （TACE） to reduce TNF-α release. These results also indicate that miR-124 is a potential therapeutic target for the treatment of inflammatory diseases.</description><subject>631/250/127</subject><subject>631/250/2504/342</subject><subject>631/250/256</subject><subject>631/337/384/331</subject><subject>Acetylcholine receptors</subject><subject>ADAM Proteins - metabolism</subject><subject>ADAM17 Protein</subject><subject>alpha7 Nicotinic Acetylcholine Receptor - metabolism</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Cell Biology</subject><subject>Cells, Cultured</subject><subject>Cholinergic Neurons - metabolism</subject><subject>Cytokines - biosynthesis</subject><subject>Cytokines - genetics</subject><subject>Cytokines - secretion</subject><subject>HEK293 Cells</subject><subject>Humans</subject><subject>Interleukin-6 - biosynthesis</subject><subject>Interleukin-6 - genetics</subject><subject>Life Sciences</subject><subject>Lipopolysaccharides - antagonists & inhibitors</subject><subject>Lipopolysaccharides - 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metabolism</topic><topic>ADAM17 Protein</topic><topic>alpha7 Nicotinic Acetylcholine Receptor - metabolism</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Cell Biology</topic><topic>Cells, Cultured</topic><topic>Cholinergic Neurons - metabolism</topic><topic>Cytokines - biosynthesis</topic><topic>Cytokines - genetics</topic><topic>Cytokines - secretion</topic><topic>HEK293 Cells</topic><topic>Humans</topic><topic>Interleukin-6 - biosynthesis</topic><topic>Interleukin-6 - genetics</topic><topic>Life Sciences</topic><topic>Lipopolysaccharides - antagonists & inhibitors</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Macrophages - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Inbred C57BL</topic><topic>MicroRNAs - metabolism</topic><topic>Original</topic><topic>original-article</topic><topic>Sepsis - chemically induced</topic><topic>Sepsis - genetics</topic><topic>Sepsis - metabolism</topic><topic>Sepsis - 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However, the intracellular mechanisms that link a7nAChR activation and pro-inflammatory cytokine production remain not well understood. In this study, we found that miR-124 is upregulated by cholinergic agonists in LPS-exposed cells and mice. Utilizing miR-124 mimic and siRNA knockdown, we demonstrated that miR-124 is a critical mediator for the cholinergic anti-inflammatory action. Furthermore, our data indicated that miR-124 modulates LPS-induced cytokine production by targeting signal transducer and activator of transcription 3 （STAT3） to decrease IL-6 production and TNF-o converting enzyme （TACE） to reduce TNF-α release. These results also indicate that miR-124 is a potential therapeutic target for the treatment of inflammatory diseases.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>23979021</pmid><doi>10.1038/cr.2013.116</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 631/250/127 631/250/2504/342 631/250/256 631/337/384/331 Acetylcholine receptors ADAM Proteins - metabolism ADAM17 Protein alpha7 Nicotinic Acetylcholine Receptor - metabolism Animals Biomedical and Life Sciences Cell Biology Cells, Cultured Cholinergic Neurons - metabolism Cytokines - biosynthesis Cytokines - genetics Cytokines - secretion HEK293 Cells Humans Interleukin-6 - biosynthesis Interleukin-6 - genetics Life Sciences Lipopolysaccharides - antagonists & inhibitors Lipopolysaccharides - pharmacology Macrophages - metabolism Mice Mice, Inbred BALB C Mice, Inbred C57BL MicroRNAs - metabolism Original original-article Sepsis - chemically induced Sepsis - genetics Sepsis - metabolism Sepsis - pathology siRNA STAT3 STAT3 Transcription Factor - metabolism TNF-α Transcription, Genetic Tumor Necrosis Factor-alpha - biosynthesis Tumor Necrosis Factor-alpha - genetics 乙酰胆碱受体 介导 抗炎作用 细胞因子 胆碱能 |
| title | MicroRNA-124 mediates the cholinergic anti-inflammatory action through inhibiting the production of pro-inflammatory cytokines |
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