Mitogen-activated protein kinase-activated protein kinase 2 regulates tumor necrosis factor-induced interleukin-6 expression via human antigen R
Background Human antigen R （HuR） is a ubiquitously expressed member of the ELAV family, and has relatively high cytoplasmic abundance in lung tissue regenerating after injury. In this study, we investigated whether mitogen-activated protein kinase （MAPK）-activated protein kinase 2 （MK2） and HuR part...
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| Veröffentlicht in: | Chinese medical journal 2013-11, Vol.126 (22), p.4322-4326 |
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| description | Background Human antigen R （HuR） is a ubiquitously expressed member of the ELAV family, and has relatively high cytoplasmic abundance in lung tissue regenerating after injury. In this study, we investigated whether mitogen-activated protein kinase （MAPK）-activated protein kinase 2 （MK2） and HuR participate in the tumor necrosis factor （TNF）-induced expression of interleukin-6 （IL-6）. Methods Human pulmonary microvascular endothelial cells were treated with TNF following short interfering RNAmediated knockdown of MK2 or HuR. Cell supernatants were collected to detect the mRNA and protein expression of IL-6 at different time points, The expression and half-life of IL-6 mRNA were then determined in cells that had been treated with actinomycin D. Finally, after knockdown of MK2, the cytoplasmic expression of HuR protein was analyzed using Western blotting. Results MK2 or HuR knockdown decreased both the mRNA and protein expression of IL-6 in TNF-stimulated cells. In MK2 knockdown cells, the half-life of IL-6 mRNA was reduced to 36 minutes, compared with 67 minutes in the control group. In HuR knockdown cells, the half-life of IL-6 mRNA decreased from 62 minutes to 24 minutes. Further analysis revealed that knockdown of MK2 resulted in reduced HuR protein expression in the cytoplasm. Conclusions MK2 regulates the TNF-induced expression of IL-6 by influencing the cytoplasmic levels of HuR. |
| doi_str_mv | 10.3760/cma.j.issn.0366-6999.20130049 |
| format | Article |
| fullrecord | <record><control><sourceid>wanfang_jour_proqu</sourceid><recordid>TN_cdi_wanfang_journals_zhcmj201322026</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><cqvip_id>47907692</cqvip_id><wanfj_id>zhcmj201322026</wanfj_id><sourcerecordid>zhcmj201322026</sourcerecordid><originalsourceid>FETCH-LOGICAL-c437t-a5e5dcb8d32385c962357d5e25ce0c27a8330b2d6845288e414fad0f385614a03</originalsourceid><addsrcrecordid>eNp1kcmO1DAURS0EoouGX0BmAWKT4HhKvGDRajFJjZAQrC2X81LlkDjVHprhK_hkHFVV71h58c71Gw5CLxtSs1aSN3Y29Vi7GH1NmJSVVErVlDSMEK4eoA0VnFZC8uYh2twDF-hJjCMhVIhWPkYXlFPWCUo36O9nl5Yd-MrY5O5Mgh4fwpLAefzDeRPhvwVMcYBdnkop4pTnJWAPNizRRTyU0BIq5_tsS9D5BGGCXIKVxPDrECBGt3h85wze59l4bHxyZQz89Sl6NJgpwrPTe4m-v3_37fpjdfPlw6frq5vKctamyggQvd12PVs3sUpSJtpeABUWiKWt6RgjW9rLjgvadcAbPpieDAWWDTeEXaJXx39_Gj8Yv9PjkoMvHfWfvZ3H9aKUEioL-PoIlvVvM8SkZxctTJPxsOSoGy5UubeSoqBvj-h6hhhg0IfgZhN-64bo1Z4u9vSoV3t6laNXOfpsr-Sfn1rl7Qz9ffqsqwAvTg32i9_dujL2meGtIq1UlP0Dkq2m3w</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1459564965</pqid></control><display><type>article</type><title>Mitogen-activated protein kinase-activated protein kinase 2 regulates tumor necrosis factor-induced interleukin-6 expression via human antigen R</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Xu, Jin ; Su, Xin ; Shi, Jia-Xin ; Sun, He ; Wu, Ting ; Shi, Yi</creator><creatorcontrib>Xu, Jin ; Su, Xin ; Shi, Jia-Xin ; Sun, He ; Wu, Ting ; Shi, Yi</creatorcontrib><description>Background Human antigen R （HuR） is a ubiquitously expressed member of the ELAV family, and has relatively high cytoplasmic abundance in lung tissue regenerating after injury. In this study, we investigated whether mitogen-activated protein kinase （MAPK）-activated protein kinase 2 （MK2） and HuR participate in the tumor necrosis factor （TNF）-induced expression of interleukin-6 （IL-6）. Methods Human pulmonary microvascular endothelial cells were treated with TNF following short interfering RNAmediated knockdown of MK2 or HuR. Cell supernatants were collected to detect the mRNA and protein expression of IL-6 at different time points, The expression and half-life of IL-6 mRNA were then determined in cells that had been treated with actinomycin D. Finally, after knockdown of MK2, the cytoplasmic expression of HuR protein was analyzed using Western blotting. Results MK2 or HuR knockdown decreased both the mRNA and protein expression of IL-6 in TNF-stimulated cells. In MK2 knockdown cells, the half-life of IL-6 mRNA was reduced to 36 minutes, compared with 67 minutes in the control group. In HuR knockdown cells, the half-life of IL-6 mRNA decreased from 62 minutes to 24 minutes. Further analysis revealed that knockdown of MK2 resulted in reduced HuR protein expression in the cytoplasm. Conclusions MK2 regulates the TNF-induced expression of IL-6 by influencing the cytoplasmic levels of HuR.</description><identifier>ISSN: 0366-6999</identifier><identifier>EISSN: 2542-5641</identifier><identifier>DOI: 10.3760/cma.j.issn.0366-6999.20130049</identifier><identifier>PMID: 24238522</identifier><language>eng</language><publisher>China: Department of Respiratory Medicine,Jiangsu Province Academy of Traditional Chinese Medicine,Nanjing, Jiangsu 210028, China%Department of Respiratory and Critical Care Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu 210002, China%Department of Respiratory Medicine, Lianyungang First People's Hospital, Lianyungang, Jiangsu 222002, China</publisher><subject>Acute Lung Injury - metabolism ; Cell Line ; ELAV Proteins - genetics ; ELAV Proteins - metabolism ; Humans ; Interleukin-6 - metabolism ; Intracellular Signaling Peptides and Proteins - genetics ; Intracellular Signaling Peptides and Proteins - metabolism ; mRNA表达 ; Protein-Serine-Threonine Kinases - genetics ; Protein-Serine-Threonine Kinases - metabolism ; Tumor Necrosis Factor-alpha - pharmacology ; Western印迹法 ; 丝裂原活化蛋白激酶 ; 抗原 ; 白细胞介素-6 ; 肺微血管内皮细胞 ; 肿瘤坏死因子 ; 诱导</subject><ispartof>Chinese medical journal, 2013-11, Vol.126 (22), p.4322-4326</ispartof><rights>Copyright © Wanfang Data Co. Ltd. All Rights Reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c437t-a5e5dcb8d32385c962357d5e25ce0c27a8330b2d6845288e414fad0f385614a03</citedby><cites>FETCH-LOGICAL-c437t-a5e5dcb8d32385c962357d5e25ce0c27a8330b2d6845288e414fad0f385614a03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/85656X/85656X.jpg</thumbnail><link.rule.ids>314,776,780,860,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24238522$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xu, Jin</creatorcontrib><creatorcontrib>Su, Xin</creatorcontrib><creatorcontrib>Shi, Jia-Xin</creatorcontrib><creatorcontrib>Sun, He</creatorcontrib><creatorcontrib>Wu, Ting</creatorcontrib><creatorcontrib>Shi, Yi</creatorcontrib><title>Mitogen-activated protein kinase-activated protein kinase 2 regulates tumor necrosis factor-induced interleukin-6 expression via human antigen R</title><title>Chinese medical journal</title><addtitle>Chinese Medical Journal</addtitle><description>Background Human antigen R （HuR） is a ubiquitously expressed member of the ELAV family, and has relatively high cytoplasmic abundance in lung tissue regenerating after injury. In this study, we investigated whether mitogen-activated protein kinase （MAPK）-activated protein kinase 2 （MK2） and HuR participate in the tumor necrosis factor （TNF）-induced expression of interleukin-6 （IL-6）. Methods Human pulmonary microvascular endothelial cells were treated with TNF following short interfering RNAmediated knockdown of MK2 or HuR. Cell supernatants were collected to detect the mRNA and protein expression of IL-6 at different time points, The expression and half-life of IL-6 mRNA were then determined in cells that had been treated with actinomycin D. Finally, after knockdown of MK2, the cytoplasmic expression of HuR protein was analyzed using Western blotting. Results MK2 or HuR knockdown decreased both the mRNA and protein expression of IL-6 in TNF-stimulated cells. In MK2 knockdown cells, the half-life of IL-6 mRNA was reduced to 36 minutes, compared with 67 minutes in the control group. In HuR knockdown cells, the half-life of IL-6 mRNA decreased from 62 minutes to 24 minutes. Further analysis revealed that knockdown of MK2 resulted in reduced HuR protein expression in the cytoplasm. Conclusions MK2 regulates the TNF-induced expression of IL-6 by influencing the cytoplasmic levels of HuR.</description><subject>Acute Lung Injury - metabolism</subject><subject>Cell Line</subject><subject>ELAV Proteins - genetics</subject><subject>ELAV Proteins - metabolism</subject><subject>Humans</subject><subject>Interleukin-6 - metabolism</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>mRNA表达</subject><subject>Protein-Serine-Threonine Kinases - genetics</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><subject>Western印迹法</subject><subject>丝裂原活化蛋白激酶</subject><subject>抗原</subject><subject>白细胞介素-6</subject><subject>肺微血管内皮细胞</subject><subject>肿瘤坏死因子</subject><subject>诱导</subject><issn>0366-6999</issn><issn>2542-5641</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kcmO1DAURS0EoouGX0BmAWKT4HhKvGDRajFJjZAQrC2X81LlkDjVHprhK_hkHFVV71h58c71Gw5CLxtSs1aSN3Y29Vi7GH1NmJSVVErVlDSMEK4eoA0VnFZC8uYh2twDF-hJjCMhVIhWPkYXlFPWCUo36O9nl5Yd-MrY5O5Mgh4fwpLAefzDeRPhvwVMcYBdnkop4pTnJWAPNizRRTyU0BIq5_tsS9D5BGGCXIKVxPDrECBGt3h85wze59l4bHxyZQz89Sl6NJgpwrPTe4m-v3_37fpjdfPlw6frq5vKctamyggQvd12PVs3sUpSJtpeABUWiKWt6RgjW9rLjgvadcAbPpieDAWWDTeEXaJXx39_Gj8Yv9PjkoMvHfWfvZ3H9aKUEioL-PoIlvVvM8SkZxctTJPxsOSoGy5UubeSoqBvj-h6hhhg0IfgZhN-64bo1Z4u9vSoV3t6laNXOfpsr-Sfn1rl7Qz9ffqsqwAvTg32i9_dujL2meGtIq1UlP0Dkq2m3w</recordid><startdate>20131120</startdate><enddate>20131120</enddate><creator>Xu, Jin</creator><creator>Su, Xin</creator><creator>Shi, Jia-Xin</creator><creator>Sun, He</creator><creator>Wu, Ting</creator><creator>Shi, Yi</creator><general>Department of Respiratory Medicine,Jiangsu Province Academy of Traditional Chinese Medicine,Nanjing, Jiangsu 210028, China%Department of Respiratory and Critical Care Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu 210002, China%Department of Respiratory Medicine, Lianyungang First People's Hospital, Lianyungang, Jiangsu 222002, China</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W91</scope><scope>~WA</scope><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>7X8</scope><scope>2B.</scope><scope>4A8</scope><scope>92I</scope><scope>93N</scope><scope>PSX</scope><scope>TCJ</scope></search><sort><creationdate>20131120</creationdate><title>Mitogen-activated protein kinase-activated protein kinase 2 regulates tumor necrosis factor-induced interleukin-6 expression via human antigen R</title><author>Xu, Jin ; Su, Xin ; Shi, Jia-Xin ; Sun, He ; Wu, Ting ; Shi, Yi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c437t-a5e5dcb8d32385c962357d5e25ce0c27a8330b2d6845288e414fad0f385614a03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Acute Lung Injury - metabolism</topic><topic>Cell Line</topic><topic>ELAV Proteins - genetics</topic><topic>ELAV Proteins - metabolism</topic><topic>Humans</topic><topic>Interleukin-6 - metabolism</topic><topic>Intracellular Signaling Peptides and Proteins - genetics</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>mRNA表达</topic><topic>Protein-Serine-Threonine Kinases - genetics</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><topic>Western印迹法</topic><topic>丝裂原活化蛋白激酶</topic><topic>抗原</topic><topic>白细胞介素-6</topic><topic>肺微血管内皮细胞</topic><topic>肿瘤坏死因子</topic><topic>诱导</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xu, Jin</creatorcontrib><creatorcontrib>Su, Xin</creatorcontrib><creatorcontrib>Shi, Jia-Xin</creatorcontrib><creatorcontrib>Sun, He</creatorcontrib><creatorcontrib>Wu, Ting</creatorcontrib><creatorcontrib>Shi, Yi</creatorcontrib><collection>中文科技期刊数据库</collection><collection>中文科技期刊数据库-CALIS站点</collection><collection>中文科技期刊数据库-7.0平台</collection><collection>中文科技期刊数据库-医药卫生</collection><collection>中文科技期刊数据库- 镜像站点</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Wanfang Data Journals - Hong Kong</collection><collection>WANFANG Data Centre</collection><collection>Wanfang Data Journals</collection><collection>万方数据期刊 - 香港版</collection><collection>China Online Journals (COJ)</collection><collection>China Online Journals (COJ)</collection><jtitle>Chinese medical journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xu, Jin</au><au>Su, Xin</au><au>Shi, Jia-Xin</au><au>Sun, He</au><au>Wu, Ting</au><au>Shi, Yi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mitogen-activated protein kinase-activated protein kinase 2 regulates tumor necrosis factor-induced interleukin-6 expression via human antigen R</atitle><jtitle>Chinese medical journal</jtitle><addtitle>Chinese Medical Journal</addtitle><date>2013-11-20</date><risdate>2013</risdate><volume>126</volume><issue>22</issue><spage>4322</spage><epage>4326</epage><pages>4322-4326</pages><issn>0366-6999</issn><eissn>2542-5641</eissn><abstract>Background Human antigen R （HuR） is a ubiquitously expressed member of the ELAV family, and has relatively high cytoplasmic abundance in lung tissue regenerating after injury. In this study, we investigated whether mitogen-activated protein kinase （MAPK）-activated protein kinase 2 （MK2） and HuR participate in the tumor necrosis factor （TNF）-induced expression of interleukin-6 （IL-6）. Methods Human pulmonary microvascular endothelial cells were treated with TNF following short interfering RNAmediated knockdown of MK2 or HuR. Cell supernatants were collected to detect the mRNA and protein expression of IL-6 at different time points, The expression and half-life of IL-6 mRNA were then determined in cells that had been treated with actinomycin D. Finally, after knockdown of MK2, the cytoplasmic expression of HuR protein was analyzed using Western blotting. Results MK2 or HuR knockdown decreased both the mRNA and protein expression of IL-6 in TNF-stimulated cells. In MK2 knockdown cells, the half-life of IL-6 mRNA was reduced to 36 minutes, compared with 67 minutes in the control group. In HuR knockdown cells, the half-life of IL-6 mRNA decreased from 62 minutes to 24 minutes. Further analysis revealed that knockdown of MK2 resulted in reduced HuR protein expression in the cytoplasm. Conclusions MK2 regulates the TNF-induced expression of IL-6 by influencing the cytoplasmic levels of HuR.</abstract><cop>China</cop><pub>Department of Respiratory Medicine,Jiangsu Province Academy of Traditional Chinese Medicine,Nanjing, Jiangsu 210028, China%Department of Respiratory and Critical Care Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu 210002, China%Department of Respiratory Medicine, Lianyungang First People's Hospital, Lianyungang, Jiangsu 222002, China</pub><pmid>24238522</pmid><doi>10.3760/cma.j.issn.0366-6999.20130049</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Acute Lung Injury - metabolism Cell Line ELAV Proteins - genetics ELAV Proteins - metabolism Humans Interleukin-6 - metabolism Intracellular Signaling Peptides and Proteins - genetics Intracellular Signaling Peptides and Proteins - metabolism mRNA表达 Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - metabolism Tumor Necrosis Factor-alpha - pharmacology Western印迹法 丝裂原活化蛋白激酶 抗原 白细胞介素-6 肺微血管内皮细胞 肿瘤坏死因子 诱导 |
| title | Mitogen-activated protein kinase-activated protein kinase 2 regulates tumor necrosis factor-induced interleukin-6 expression via human antigen R |
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