MiR-23a inhibited IL-17-mediated proinflammatory mediators expression via targeting IKKα in articular chondrocytes
The inflammatory cytokine interleukin 17 (IL-17) is an important contributor of rheumatoid arthritis (RA) chronicity. Although several microRNAs (miRNAs) have been shown to regulate RA pathogenesis, the function of miRNAs in articular chondrocytes during rheumatoid arthritis pathogenesis is unclear....
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| Veröffentlicht in: | International immunopharmacology 2017-02, Vol.43, p.1-6 |
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| creator | Hu, Junzheng Zhai, Chenjun Hu, Jiaojiao Li, Zeng Fei, Hao Wang, Zhen Fan, Weimin |
| description | The inflammatory cytokine interleukin 17 (IL-17) is an important contributor of rheumatoid arthritis (RA) chronicity. Although several microRNAs (miRNAs) have been shown to regulate RA pathogenesis, the function of miRNAs in articular chondrocytes during rheumatoid arthritis pathogenesis is unclear. Here we showed that miR-23a was downregulated in articular cartilage tissues from rheumatoid arthritis patients. MiR-23a suppressed IL-17 inflammatory cytokine–induced NF-κB activation and several proinflammatory mediators expression, such as cytokine IL-6, chemokine MCP-1, and matrix metalloproteinase MMP-3 in articular chondrocytes. Furthermore, we found that the miR-23a expression was inversely correlated with IKKα expression in articular cartilage tissues from rheumatoid arthritis patients. We identified that IKKα was the direct target of miR-23a and miR-23a inhibited IL-17-mediated proinflammatory mediators expression via targeting the IKKα in primary articular chondrocytes. Together, our study provides the first evidence of a role for miR-23a regulated IL-17-mediated proinflammatory mediators expression in rheumatoid arthritis by directly targeting IKKα. Our findings provide novel evidence that may be useful for future studies exploring therapeutic approaches for rheumatoid arthritis by targeting miR-23a. Thus, miR-23a may be a common therapeutic target for rheumatoid arthritis.
•miR-23a expression was decreased in rheumatoid arthritis.•miR-23a suppressed IL-17-mediated proinflammatory mediators expression.•miR-23a expression was inversely correlated with IKKα expression.•miR-23a inhibited IL-17-mediated proinflammatory mediators expression via targeting the IKKα. |
| doi_str_mv | 10.1016/j.intimp.2016.11.031 |
| format | Article |
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•miR-23a expression was decreased in rheumatoid arthritis.•miR-23a suppressed IL-17-mediated proinflammatory mediators expression.•miR-23a expression was inversely correlated with IKKα expression.•miR-23a inhibited IL-17-mediated proinflammatory mediators expression via targeting the IKKα.</description><identifier>ISSN: 1567-5769</identifier><identifier>EISSN: 1878-1705</identifier><identifier>DOI: 10.1016/j.intimp.2016.11.031</identifier><identifier>PMID: 27936459</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Arthritis ; Arthritis, Rheumatoid - genetics ; Arthritis, Rheumatoid - immunology ; Arthritis, Rheumatoid - therapy ; Cartilage ; Cartilage (articular) ; Cartilage, Articular - pathology ; Cells, Cultured ; Chemokine CCL2 - genetics ; Chemokine CCL2 - metabolism ; Chondrocytes ; Chondrocytes - physiology ; Cytokines ; Gene Expression Regulation - genetics ; Humans ; I-kappa B Kinase - genetics ; I-kappa B Kinase - metabolism ; IKKα ; Inflammation ; Inflammation Mediators - metabolism ; Interleukin 17 ; Interleukin 6 ; Interleukin-17 - immunology ; Interleukin-6 - genetics ; Interleukin-6 - metabolism ; Matrix metalloproteinase ; Matrix Metalloproteinase 3 - genetics ; Matrix Metalloproteinase 3 - metabolism ; Metalloproteinase ; MicroRNAs - genetics ; miR-23a ; miRNA ; Molecular Targeted Therapy ; Monocyte chemoattractant protein 1 ; Pathogenesis ; Patients ; Rheumatoid arthritis ; Stromelysin 1 ; Tissues</subject><ispartof>International immunopharmacology, 2017-02, Vol.43, p.1-6</ispartof><rights>2016</rights><rights>Copyright © 2016. Published by Elsevier B.V.</rights><rights>Copyright Elsevier BV Feb 2017</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-70a27d1dd6434570dcd045a8aed97473ae759b5dcdb5a1c89bf34566092c73eb3</citedby><cites>FETCH-LOGICAL-c390t-70a27d1dd6434570dcd045a8aed97473ae759b5dcdb5a1c89bf34566092c73eb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.intimp.2016.11.031$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27929,27930,46000</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27936459$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hu, Junzheng</creatorcontrib><creatorcontrib>Zhai, Chenjun</creatorcontrib><creatorcontrib>Hu, Jiaojiao</creatorcontrib><creatorcontrib>Li, Zeng</creatorcontrib><creatorcontrib>Fei, Hao</creatorcontrib><creatorcontrib>Wang, Zhen</creatorcontrib><creatorcontrib>Fan, Weimin</creatorcontrib><title>MiR-23a inhibited IL-17-mediated proinflammatory mediators expression via targeting IKKα in articular chondrocytes</title><title>International immunopharmacology</title><addtitle>Int Immunopharmacol</addtitle><description>The inflammatory cytokine interleukin 17 (IL-17) is an important contributor of rheumatoid arthritis (RA) chronicity. Although several microRNAs (miRNAs) have been shown to regulate RA pathogenesis, the function of miRNAs in articular chondrocytes during rheumatoid arthritis pathogenesis is unclear. Here we showed that miR-23a was downregulated in articular cartilage tissues from rheumatoid arthritis patients. MiR-23a suppressed IL-17 inflammatory cytokine–induced NF-κB activation and several proinflammatory mediators expression, such as cytokine IL-6, chemokine MCP-1, and matrix metalloproteinase MMP-3 in articular chondrocytes. Furthermore, we found that the miR-23a expression was inversely correlated with IKKα expression in articular cartilage tissues from rheumatoid arthritis patients. We identified that IKKα was the direct target of miR-23a and miR-23a inhibited IL-17-mediated proinflammatory mediators expression via targeting the IKKα in primary articular chondrocytes. Together, our study provides the first evidence of a role for miR-23a regulated IL-17-mediated proinflammatory mediators expression in rheumatoid arthritis by directly targeting IKKα. Our findings provide novel evidence that may be useful for future studies exploring therapeutic approaches for rheumatoid arthritis by targeting miR-23a. Thus, miR-23a may be a common therapeutic target for rheumatoid arthritis.
•miR-23a expression was decreased in rheumatoid arthritis.•miR-23a suppressed IL-17-mediated proinflammatory mediators expression.•miR-23a expression was inversely correlated with IKKα expression.•miR-23a inhibited IL-17-mediated proinflammatory mediators expression via targeting the IKKα.</description><subject>Arthritis</subject><subject>Arthritis, Rheumatoid - genetics</subject><subject>Arthritis, Rheumatoid - immunology</subject><subject>Arthritis, Rheumatoid - therapy</subject><subject>Cartilage</subject><subject>Cartilage (articular)</subject><subject>Cartilage, Articular - pathology</subject><subject>Cells, Cultured</subject><subject>Chemokine CCL2 - genetics</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Chondrocytes</subject><subject>Chondrocytes - physiology</subject><subject>Cytokines</subject><subject>Gene Expression Regulation - genetics</subject><subject>Humans</subject><subject>I-kappa B Kinase - genetics</subject><subject>I-kappa B Kinase - metabolism</subject><subject>IKKα</subject><subject>Inflammation</subject><subject>Inflammation Mediators - metabolism</subject><subject>Interleukin 17</subject><subject>Interleukin 6</subject><subject>Interleukin-17 - immunology</subject><subject>Interleukin-6 - genetics</subject><subject>Interleukin-6 - metabolism</subject><subject>Matrix metalloproteinase</subject><subject>Matrix Metalloproteinase 3 - genetics</subject><subject>Matrix Metalloproteinase 3 - metabolism</subject><subject>Metalloproteinase</subject><subject>MicroRNAs - genetics</subject><subject>miR-23a</subject><subject>miRNA</subject><subject>Molecular Targeted Therapy</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Pathogenesis</subject><subject>Patients</subject><subject>Rheumatoid arthritis</subject><subject>Stromelysin 1</subject><subject>Tissues</subject><issn>1567-5769</issn><issn>1878-1705</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc2OFCEUhYnROGPrGxhD4sZNldyigGJjYib-dKaNidE1oYCeoVMFLVAT-7F8EZ9JOjW6cOEK7uW7BzgHoedAWiDAXx9aH4qfj21XqxagJRQeoEsYxNCAIOxh3TMuGia4vEBPcj4QUvs9PEYXnZCU90xeovzJf2k6qrEPt370xVm83dX5ZnbW63N5TNGH_aTnWZeYTng9iClj9-OYXM4-BnznNS463bjiww3eXl__-lkVsU7Fm2XSCZvbGGyK5lRcfooe7fWU3bP7dYO-vX_39epjs_v8YXv1dtcYKklpBNGdsGAt72nPBLHGkp7pQTsrRS-odoLJkdX2yDSYQY77ynFOZGcEdSPdoFerbv3C98XlomafjZsmHVxcsoKBdZzJnouKvvwHPcQlhfo6BZIClwKqZRvUr5RJMefk9uqY_KzTSQFR51DUQa2hqHMoCkDVUOrYi3vxZazu_R36k0IF3qyAq27ceZdUNt4FU51OzhRlo___Db8BFN2g1A</recordid><startdate>201702</startdate><enddate>201702</enddate><creator>Hu, Junzheng</creator><creator>Zhai, Chenjun</creator><creator>Hu, Jiaojiao</creator><creator>Li, Zeng</creator><creator>Fei, Hao</creator><creator>Wang, Zhen</creator><creator>Fan, Weimin</creator><general>Elsevier B.V</general><general>Elsevier BV</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>7QO</scope><scope>7T5</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>201702</creationdate><title>MiR-23a inhibited IL-17-mediated proinflammatory mediators expression via targeting IKKα in articular chondrocytes</title><author>Hu, Junzheng ; Zhai, Chenjun ; Hu, Jiaojiao ; Li, Zeng ; Fei, Hao ; Wang, Zhen ; Fan, Weimin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-70a27d1dd6434570dcd045a8aed97473ae759b5dcdb5a1c89bf34566092c73eb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Arthritis</topic><topic>Arthritis, Rheumatoid - genetics</topic><topic>Arthritis, Rheumatoid - immunology</topic><topic>Arthritis, Rheumatoid - therapy</topic><topic>Cartilage</topic><topic>Cartilage (articular)</topic><topic>Cartilage, Articular - pathology</topic><topic>Cells, Cultured</topic><topic>Chemokine CCL2 - genetics</topic><topic>Chemokine CCL2 - metabolism</topic><topic>Chondrocytes</topic><topic>Chondrocytes - physiology</topic><topic>Cytokines</topic><topic>Gene Expression Regulation - genetics</topic><topic>Humans</topic><topic>I-kappa B Kinase - genetics</topic><topic>I-kappa B Kinase - metabolism</topic><topic>IKKα</topic><topic>Inflammation</topic><topic>Inflammation Mediators - metabolism</topic><topic>Interleukin 17</topic><topic>Interleukin 6</topic><topic>Interleukin-17 - immunology</topic><topic>Interleukin-6 - genetics</topic><topic>Interleukin-6 - metabolism</topic><topic>Matrix metalloproteinase</topic><topic>Matrix Metalloproteinase 3 - genetics</topic><topic>Matrix Metalloproteinase 3 - metabolism</topic><topic>Metalloproteinase</topic><topic>MicroRNAs - genetics</topic><topic>miR-23a</topic><topic>miRNA</topic><topic>Molecular Targeted Therapy</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Pathogenesis</topic><topic>Patients</topic><topic>Rheumatoid arthritis</topic><topic>Stromelysin 1</topic><topic>Tissues</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hu, Junzheng</creatorcontrib><creatorcontrib>Zhai, Chenjun</creatorcontrib><creatorcontrib>Hu, Jiaojiao</creatorcontrib><creatorcontrib>Li, Zeng</creatorcontrib><creatorcontrib>Fei, Hao</creatorcontrib><creatorcontrib>Wang, Zhen</creatorcontrib><creatorcontrib>Fan, Weimin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Immunology Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International immunopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hu, Junzheng</au><au>Zhai, Chenjun</au><au>Hu, Jiaojiao</au><au>Li, Zeng</au><au>Fei, Hao</au><au>Wang, Zhen</au><au>Fan, Weimin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MiR-23a inhibited IL-17-mediated proinflammatory mediators expression via targeting IKKα in articular chondrocytes</atitle><jtitle>International immunopharmacology</jtitle><addtitle>Int Immunopharmacol</addtitle><date>2017-02</date><risdate>2017</risdate><volume>43</volume><spage>1</spage><epage>6</epage><pages>1-6</pages><issn>1567-5769</issn><eissn>1878-1705</eissn><abstract>The inflammatory cytokine interleukin 17 (IL-17) is an important contributor of rheumatoid arthritis (RA) chronicity. Although several microRNAs (miRNAs) have been shown to regulate RA pathogenesis, the function of miRNAs in articular chondrocytes during rheumatoid arthritis pathogenesis is unclear. Here we showed that miR-23a was downregulated in articular cartilage tissues from rheumatoid arthritis patients. MiR-23a suppressed IL-17 inflammatory cytokine–induced NF-κB activation and several proinflammatory mediators expression, such as cytokine IL-6, chemokine MCP-1, and matrix metalloproteinase MMP-3 in articular chondrocytes. Furthermore, we found that the miR-23a expression was inversely correlated with IKKα expression in articular cartilage tissues from rheumatoid arthritis patients. We identified that IKKα was the direct target of miR-23a and miR-23a inhibited IL-17-mediated proinflammatory mediators expression via targeting the IKKα in primary articular chondrocytes. Together, our study provides the first evidence of a role for miR-23a regulated IL-17-mediated proinflammatory mediators expression in rheumatoid arthritis by directly targeting IKKα. Our findings provide novel evidence that may be useful for future studies exploring therapeutic approaches for rheumatoid arthritis by targeting miR-23a. Thus, miR-23a may be a common therapeutic target for rheumatoid arthritis.
•miR-23a expression was decreased in rheumatoid arthritis.•miR-23a suppressed IL-17-mediated proinflammatory mediators expression.•miR-23a expression was inversely correlated with IKKα expression.•miR-23a inhibited IL-17-mediated proinflammatory mediators expression via targeting the IKKα.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>27936459</pmid><doi>10.1016/j.intimp.2016.11.031</doi><tpages>6</tpages></addata></record> |
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| subjects | Arthritis Arthritis, Rheumatoid - genetics Arthritis, Rheumatoid - immunology Arthritis, Rheumatoid - therapy Cartilage Cartilage (articular) Cartilage, Articular - pathology Cells, Cultured Chemokine CCL2 - genetics Chemokine CCL2 - metabolism Chondrocytes Chondrocytes - physiology Cytokines Gene Expression Regulation - genetics Humans I-kappa B Kinase - genetics I-kappa B Kinase - metabolism IKKα Inflammation Inflammation Mediators - metabolism Interleukin 17 Interleukin 6 Interleukin-17 - immunology Interleukin-6 - genetics Interleukin-6 - metabolism Matrix metalloproteinase Matrix Metalloproteinase 3 - genetics Matrix Metalloproteinase 3 - metabolism Metalloproteinase MicroRNAs - genetics miR-23a miRNA Molecular Targeted Therapy Monocyte chemoattractant protein 1 Pathogenesis Patients Rheumatoid arthritis Stromelysin 1 Tissues |
| title | MiR-23a inhibited IL-17-mediated proinflammatory mediators expression via targeting IKKα in articular chondrocytes |
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