Identification of MicroRNAs Dysregulated in CD14 Gene Silencing RAW264.7 Macrophage Cells
A cluster of differentiation antigen 14 (CD14) is involved in lipopolysaccharide (LPS)-induced proinflammatory cytokine release and LPS-induced septic shock. MicroRNAs (miRNAs) are short non-coding RNAs that are involved in the epigenetic regulation of cellular process and bacterial infection. Our p...
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| Veröffentlicht in: | Inflammation 2014-02, Vol.37 (1), p.287-294 |
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| creator | Du, Li Rong, Hui Cheng, Ying Guo, Shiyu Shi, Qiaoyun Jia, Xiaoxiao Zhu, Huapei Hao, Yongchang Xu, Kailian Zhang, Jianing Jiao, Hanwei Zhao, Tianjing Zhang, Hui Chen, Chuangfu Wang, Fengyang |
| description | A cluster of differentiation antigen 14 (CD14) is involved in lipopolysaccharide (LPS)-induced proinflammatory cytokine release and LPS-induced septic shock. MicroRNAs (miRNAs) are short non-coding RNAs that are involved in the epigenetic regulation of cellular process and bacterial infection. Our previous study indicated that siRNA against CD14 effectively inhibited LPS-induced tumor necrosis factor alpha, chemokine (C-X-C motif) ligand 2, interleukin-6 release, and NO production. To identify miRNAs which are affected by CD14 gene silencing and dissect the mechanisms of the attenuating of LPS-induced damaging immune activation more clearly, based on the CD14 knockdown RAW264.7 macrophage cell line established in our previous study, miRNAs expression profiling of CD14 knockdown RAW264.7 cells were analyzed with miRNA microarray and validated by qRT-PCR, the potential targets were predicted and subjected to gene ontology (GO) pathway and biological processes analysis. We demonstrated for the first time that CD14 knockdown significantly changed the expression of 199a-3p, miR-199a-5p, and miR-21-5p in RAW264.7 cells, and significantly enriched GO terms in the predicted target genes of these miRNAs were apoptosis process, immune response, inflammatory response, innate immune response, anti-apoptosis, cytokine production, and cytokine-mediated signaling pathway. These findings may improve our understanding about functional mechanism of miRNAs in the attenuating of LPS-induced damaging immune activation more clearly. |
| doi_str_mv | 10.1007/s10753-013-9739-3 |
| format | Article |
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MicroRNAs (miRNAs) are short non-coding RNAs that are involved in the epigenetic regulation of cellular process and bacterial infection. Our previous study indicated that siRNA against CD14 effectively inhibited LPS-induced tumor necrosis factor alpha, chemokine (C-X-C motif) ligand 2, interleukin-6 release, and NO production. To identify miRNAs which are affected by CD14 gene silencing and dissect the mechanisms of the attenuating of LPS-induced damaging immune activation more clearly, based on the CD14 knockdown RAW264.7 macrophage cell line established in our previous study, miRNAs expression profiling of CD14 knockdown RAW264.7 cells were analyzed with miRNA microarray and validated by qRT-PCR, the potential targets were predicted and subjected to gene ontology (GO) pathway and biological processes analysis. We demonstrated for the first time that CD14 knockdown significantly changed the expression of 199a-3p, miR-199a-5p, and miR-21-5p in RAW264.7 cells, and significantly enriched GO terms in the predicted target genes of these miRNAs were apoptosis process, immune response, inflammatory response, innate immune response, anti-apoptosis, cytokine production, and cytokine-mediated signaling pathway. These findings may improve our understanding about functional mechanism of miRNAs in the attenuating of LPS-induced damaging immune activation more clearly.</description><identifier>ISSN: 0360-3997</identifier><identifier>EISSN: 1573-2576</identifier><identifier>DOI: 10.1007/s10753-013-9739-3</identifier><identifier>PMID: 24062059</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Apoptosis ; Apoptosis - genetics ; Biomedicine ; CD14 antigen ; Cell differentiation ; Cell Line ; Cytokines ; Cytokines - biosynthesis ; Cytokines - genetics ; DNA microarrays ; Epigenetics ; Gene Knockout Techniques ; Gene silencing ; Immune response ; Immunology ; Inflammation ; Inflammation - genetics ; Inflammation - immunology ; Interleukin 6 ; Internal Medicine ; Lipopolysaccharide Receptors - genetics ; Lipopolysaccharides ; Macrophages ; Macrophages - cytology ; Macrophages - immunology ; Mice ; MicroRNAs ; MicroRNAs - biosynthesis ; MicroRNAs - genetics ; miRNA ; Pathology ; Pharmacology/Toxicology ; Rheumatology ; Septic shock ; Shock, Septic - chemically induced ; Shock, Septic - genetics ; Shock, Septic - immunology ; Signal transduction ; siRNA ; Tumor necrosis factor-α</subject><ispartof>Inflammation, 2014-02, Vol.37 (1), p.287-294</ispartof><rights>Springer Science+Business Media New York 2013</rights><rights>Springer Science+Business Media New York 2013.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-98293fce7dd33204d64c0e3ef4de193c774181739f11fbde7219135f345b4fc3</citedby><cites>FETCH-LOGICAL-c405t-98293fce7dd33204d64c0e3ef4de193c774181739f11fbde7219135f345b4fc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10753-013-9739-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10753-013-9739-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27926,27927,41490,42559,51321</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24062059$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Du, Li</creatorcontrib><creatorcontrib>Rong, Hui</creatorcontrib><creatorcontrib>Cheng, Ying</creatorcontrib><creatorcontrib>Guo, Shiyu</creatorcontrib><creatorcontrib>Shi, Qiaoyun</creatorcontrib><creatorcontrib>Jia, Xiaoxiao</creatorcontrib><creatorcontrib>Zhu, Huapei</creatorcontrib><creatorcontrib>Hao, Yongchang</creatorcontrib><creatorcontrib>Xu, Kailian</creatorcontrib><creatorcontrib>Zhang, Jianing</creatorcontrib><creatorcontrib>Jiao, Hanwei</creatorcontrib><creatorcontrib>Zhao, Tianjing</creatorcontrib><creatorcontrib>Zhang, Hui</creatorcontrib><creatorcontrib>Chen, Chuangfu</creatorcontrib><creatorcontrib>Wang, Fengyang</creatorcontrib><title>Identification of MicroRNAs Dysregulated in CD14 Gene Silencing RAW264.7 Macrophage Cells</title><title>Inflammation</title><addtitle>Inflammation</addtitle><addtitle>Inflammation</addtitle><description>A cluster of differentiation antigen 14 (CD14) is involved in lipopolysaccharide (LPS)-induced proinflammatory cytokine release and LPS-induced septic shock. MicroRNAs (miRNAs) are short non-coding RNAs that are involved in the epigenetic regulation of cellular process and bacterial infection. Our previous study indicated that siRNA against CD14 effectively inhibited LPS-induced tumor necrosis factor alpha, chemokine (C-X-C motif) ligand 2, interleukin-6 release, and NO production. To identify miRNAs which are affected by CD14 gene silencing and dissect the mechanisms of the attenuating of LPS-induced damaging immune activation more clearly, based on the CD14 knockdown RAW264.7 macrophage cell line established in our previous study, miRNAs expression profiling of CD14 knockdown RAW264.7 cells were analyzed with miRNA microarray and validated by qRT-PCR, the potential targets were predicted and subjected to gene ontology (GO) pathway and biological processes analysis. We demonstrated for the first time that CD14 knockdown significantly changed the expression of 199a-3p, miR-199a-5p, and miR-21-5p in RAW264.7 cells, and significantly enriched GO terms in the predicted target genes of these miRNAs were apoptosis process, immune response, inflammatory response, innate immune response, anti-apoptosis, cytokine production, and cytokine-mediated signaling pathway. These findings may improve our understanding about functional mechanism of miRNAs in the attenuating of LPS-induced damaging immune activation more clearly.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Biomedicine</subject><subject>CD14 antigen</subject><subject>Cell differentiation</subject><subject>Cell Line</subject><subject>Cytokines</subject><subject>Cytokines - biosynthesis</subject><subject>Cytokines - genetics</subject><subject>DNA microarrays</subject><subject>Epigenetics</subject><subject>Gene Knockout Techniques</subject><subject>Gene silencing</subject><subject>Immune response</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Inflammation - genetics</subject><subject>Inflammation - immunology</subject><subject>Interleukin 6</subject><subject>Internal Medicine</subject><subject>Lipopolysaccharide Receptors - genetics</subject><subject>Lipopolysaccharides</subject><subject>Macrophages</subject><subject>Macrophages - cytology</subject><subject>Macrophages - immunology</subject><subject>Mice</subject><subject>MicroRNAs</subject><subject>MicroRNAs - biosynthesis</subject><subject>MicroRNAs - genetics</subject><subject>miRNA</subject><subject>Pathology</subject><subject>Pharmacology/Toxicology</subject><subject>Rheumatology</subject><subject>Septic shock</subject><subject>Shock, Septic - chemically induced</subject><subject>Shock, Septic - genetics</subject><subject>Shock, Septic - immunology</subject><subject>Signal transduction</subject><subject>siRNA</subject><subject>Tumor necrosis factor-α</subject><issn>0360-3997</issn><issn>1573-2576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kE1r3DAQhkVoSTZpfkAuRdBLL041Gtmyjsum-YB8QBoIOQmvPNoqeOWtZR_y76Nl01ICOekwz7ya92HsBMQpCKF_JBC6xEIAFkajKXCPzaDUWMhSV5_YTGAlCjRGH7DDlJ6FELWpcZ8dSCUqKUozY09XLcUx-OCaMfSR957fBDf097fzxM9e0kCrqWtGanmIfHEGil9QJP4rdBRdiCt-P3-UlTrV_KbJa5vfzYr4groufWGffdMlOn57j9jD-c-HxWVxfXdxtZhfF06JcixMLQ16R7ptEaVQbaWcICSvWgKDTmsFNeR2HsAvW9ISDGDpUZVL5R0ese-72M3Q_5kojXYdkssHNJH6KVkos6kqZ2BGv71Dn_tpiPk4C8qABK1qmSnYUblOyv293Qxh3QwvFoTdarc77TZrt1vtdpv89S15Wq6p_bfx13MG5A5IeRRXNPz39YepryR1idY</recordid><startdate>20140201</startdate><enddate>20140201</enddate><creator>Du, Li</creator><creator>Rong, Hui</creator><creator>Cheng, Ying</creator><creator>Guo, Shiyu</creator><creator>Shi, Qiaoyun</creator><creator>Jia, Xiaoxiao</creator><creator>Zhu, Huapei</creator><creator>Hao, Yongchang</creator><creator>Xu, Kailian</creator><creator>Zhang, Jianing</creator><creator>Jiao, Hanwei</creator><creator>Zhao, Tianjing</creator><creator>Zhang, Hui</creator><creator>Chen, Chuangfu</creator><creator>Wang, Fengyang</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20140201</creationdate><title>Identification of MicroRNAs Dysregulated in CD14 Gene Silencing RAW264.7 Macrophage Cells</title><author>Du, Li ; Rong, Hui ; Cheng, Ying ; Guo, Shiyu ; Shi, Qiaoyun ; Jia, Xiaoxiao ; Zhu, Huapei ; Hao, Yongchang ; Xu, Kailian ; Zhang, Jianing ; Jiao, Hanwei ; Zhao, Tianjing ; Zhang, Hui ; Chen, Chuangfu ; Wang, Fengyang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c405t-98293fce7dd33204d64c0e3ef4de193c774181739f11fbde7219135f345b4fc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Biomedicine</topic><topic>CD14 antigen</topic><topic>Cell differentiation</topic><topic>Cell Line</topic><topic>Cytokines</topic><topic>Cytokines - biosynthesis</topic><topic>Cytokines - genetics</topic><topic>DNA microarrays</topic><topic>Epigenetics</topic><topic>Gene Knockout Techniques</topic><topic>Gene silencing</topic><topic>Immune response</topic><topic>Immunology</topic><topic>Inflammation</topic><topic>Inflammation - genetics</topic><topic>Inflammation - immunology</topic><topic>Interleukin 6</topic><topic>Internal Medicine</topic><topic>Lipopolysaccharide Receptors - genetics</topic><topic>Lipopolysaccharides</topic><topic>Macrophages</topic><topic>Macrophages - cytology</topic><topic>Macrophages - immunology</topic><topic>Mice</topic><topic>MicroRNAs</topic><topic>MicroRNAs - biosynthesis</topic><topic>MicroRNAs - genetics</topic><topic>miRNA</topic><topic>Pathology</topic><topic>Pharmacology/Toxicology</topic><topic>Rheumatology</topic><topic>Septic shock</topic><topic>Shock, Septic - chemically induced</topic><topic>Shock, Septic - genetics</topic><topic>Shock, Septic - immunology</topic><topic>Signal transduction</topic><topic>siRNA</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Du, Li</creatorcontrib><creatorcontrib>Rong, Hui</creatorcontrib><creatorcontrib>Cheng, Ying</creatorcontrib><creatorcontrib>Guo, Shiyu</creatorcontrib><creatorcontrib>Shi, Qiaoyun</creatorcontrib><creatorcontrib>Jia, Xiaoxiao</creatorcontrib><creatorcontrib>Zhu, Huapei</creatorcontrib><creatorcontrib>Hao, Yongchang</creatorcontrib><creatorcontrib>Xu, Kailian</creatorcontrib><creatorcontrib>Zhang, Jianing</creatorcontrib><creatorcontrib>Jiao, Hanwei</creatorcontrib><creatorcontrib>Zhao, Tianjing</creatorcontrib><creatorcontrib>Zhang, Hui</creatorcontrib><creatorcontrib>Chen, Chuangfu</creatorcontrib><creatorcontrib>Wang, Fengyang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Du, Li</au><au>Rong, Hui</au><au>Cheng, Ying</au><au>Guo, Shiyu</au><au>Shi, Qiaoyun</au><au>Jia, Xiaoxiao</au><au>Zhu, Huapei</au><au>Hao, Yongchang</au><au>Xu, Kailian</au><au>Zhang, Jianing</au><au>Jiao, Hanwei</au><au>Zhao, Tianjing</au><au>Zhang, Hui</au><au>Chen, Chuangfu</au><au>Wang, Fengyang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Identification of MicroRNAs Dysregulated in CD14 Gene Silencing RAW264.7 Macrophage Cells</atitle><jtitle>Inflammation</jtitle><stitle>Inflammation</stitle><addtitle>Inflammation</addtitle><date>2014-02-01</date><risdate>2014</risdate><volume>37</volume><issue>1</issue><spage>287</spage><epage>294</epage><pages>287-294</pages><issn>0360-3997</issn><eissn>1573-2576</eissn><abstract>A cluster of differentiation antigen 14 (CD14) is involved in lipopolysaccharide (LPS)-induced proinflammatory cytokine release and LPS-induced septic shock. MicroRNAs (miRNAs) are short non-coding RNAs that are involved in the epigenetic regulation of cellular process and bacterial infection. Our previous study indicated that siRNA against CD14 effectively inhibited LPS-induced tumor necrosis factor alpha, chemokine (C-X-C motif) ligand 2, interleukin-6 release, and NO production. To identify miRNAs which are affected by CD14 gene silencing and dissect the mechanisms of the attenuating of LPS-induced damaging immune activation more clearly, based on the CD14 knockdown RAW264.7 macrophage cell line established in our previous study, miRNAs expression profiling of CD14 knockdown RAW264.7 cells were analyzed with miRNA microarray and validated by qRT-PCR, the potential targets were predicted and subjected to gene ontology (GO) pathway and biological processes analysis. We demonstrated for the first time that CD14 knockdown significantly changed the expression of 199a-3p, miR-199a-5p, and miR-21-5p in RAW264.7 cells, and significantly enriched GO terms in the predicted target genes of these miRNAs were apoptosis process, immune response, inflammatory response, innate immune response, anti-apoptosis, cytokine production, and cytokine-mediated signaling pathway. These findings may improve our understanding about functional mechanism of miRNAs in the attenuating of LPS-induced damaging immune activation more clearly.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>24062059</pmid><doi>10.1007/s10753-013-9739-3</doi><tpages>8</tpages></addata></record> |
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| subjects | Animals Apoptosis Apoptosis - genetics Biomedicine CD14 antigen Cell differentiation Cell Line Cytokines Cytokines - biosynthesis Cytokines - genetics DNA microarrays Epigenetics Gene Knockout Techniques Gene silencing Immune response Immunology Inflammation Inflammation - genetics Inflammation - immunology Interleukin 6 Internal Medicine Lipopolysaccharide Receptors - genetics Lipopolysaccharides Macrophages Macrophages - cytology Macrophages - immunology Mice MicroRNAs MicroRNAs - biosynthesis MicroRNAs - genetics miRNA Pathology Pharmacology/Toxicology Rheumatology Septic shock Shock, Septic - chemically induced Shock, Septic - genetics Shock, Septic - immunology Signal transduction siRNA Tumor necrosis factor-α |
| title | Identification of MicroRNAs Dysregulated in CD14 Gene Silencing RAW264.7 Macrophage Cells |
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