MicroRNA‐193b‐3p regulates matrix metalloproteinase 19 expression in interleukin‐1β‐induced human chondrocytes
Micro(mi)RNAs are small, non‐coding RNA molecules known to play a significant role in osteoarthritis (OA) initiation and development, and similar to matrix metalloproteinases (MMPs), they participate in cartilage degeneration and cleave multiple extracellular matrices. The aim of this study was to d...
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Veröffentlicht in: | Journal of cellular biochemistry 2018-06, Vol.119 (6), p.4775-4782 |
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creator | Chang, Zong‐kun Meng, Fan‐gang Zhang, Zhi‐qi Mao, Gu‐ping Huang, Zhi‐yu Liao, Wei‐ming He, Ai‐shan |
description | Micro(mi)RNAs are small, non‐coding RNA molecules known to play a significant role in osteoarthritis (OA) initiation and development, and similar to matrix metalloproteinases (MMPs), they participate in cartilage degeneration and cleave multiple extracellular matrices. The aim of this study was to determine whether the expression of MMP‐19 in interleukin (IL)‐1β‐induced human chondrocytes is directly regulated by miR‐193b‐3p. Expression levels of miR‐193b‐3p and MMP‐19 in normal and osteoarthritis (OA) human cartilage, and interleukin‐1 β (IL‐1β)‐induced human chondrocytes were determined by real‐time polymerase chain reaction. Additionally, expression level of MMP‐19 in IL‐1β‐induced human chondrocytes was estimated by Western blotting and immunohistochemistry analyses. The effect of miR‐193b‐3p on MMP‐19 expression was evaluated using transient transfection of normal human chondrocytes with miR‐193b‐3p mimic or its antisense inhibitor (miR‐193b‐3p inhibitor), and siMMP‐19. The putative binding site of miR‐193b‐3p in the 3′‐untranslated region (UTR) of MMP‐19 mRNA was validated by luciferase reporter assay. miR‐193b‐3p expression was reduced in OA cartilage compared to that in normal chondrocytes, while the opposite was observed for MMP‐19. Upregulation of MMP‐19 expression was correlated with downregulation of miR‐193b‐3p in IL‐1β‐stimulated normal chondrocytes. Increase in miR‐193b‐3p levels was associated with silencing of MMP‐19. Overexpression of miR‐193b‐3p suppressed the activity of the reporter construct containing the 3′‐UTR of human MMP‐19 mRNA and inhibited the IL‐1β‐induced expression of MMP‐19 and iNOS in chondrocytes, while treatment with miR‐193b‐3p inhibitor enhanced MMP‐19 expression. MiR‐193b‐3p is an important regulator of MMP‐19 in human chondrocytes and may relieve the inflammatory response in OA.
This study investigated the relationship of miR‐193b‐3p and MMP‐19 in osteoarthritis cartilage, and determined that microRNA‐193b‐3p (miR‐193b‐3p) regulates MMP‐19 expression in IL‐1β‐stimulated normal chondrocytes directly. |
doi_str_mv | 10.1002/jcb.26669 |
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This study investigated the relationship of miR‐193b‐3p and MMP‐19 in osteoarthritis cartilage, and determined that microRNA‐193b‐3p (miR‐193b‐3p) regulates MMP‐19 expression in IL‐1β‐stimulated normal chondrocytes directly.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.26669</identifier><identifier>PMID: 29323744</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>3' Untranslated regions ; Addition polymerization ; Antisense RNA ; Arthritis ; Binding sites ; Biocompatibility ; Biomedical materials ; Cartilage ; Cartilage diseases ; Chondrocytes ; Cytokines ; Degeneration ; Gene expression ; IL-1β ; Immunohistochemistry ; Inflammation ; Inflammatory response ; Inhibitors ; Interleukins ; Matrix metalloproteinase ; Matrix metalloproteinases ; Metalloproteinase ; miRNA ; miR‐193b‐3p ; MMP‐19 ; mRNA ; Nitric-oxide synthase ; Osteoarthritis ; Polymerase chain reaction ; Ribonucleic acid ; RNA ; Test systems ; Transfection ; Western blotting</subject><ispartof>Journal of cellular biochemistry, 2018-06, Vol.119 (6), p.4775-4782</ispartof><rights>2018 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3539-7262dbb6dace58537d834dabc4ba43964ab0b028892ae7aadf92f2cf7de3fbf73</citedby><cites>FETCH-LOGICAL-c3539-7262dbb6dace58537d834dabc4ba43964ab0b028892ae7aadf92f2cf7de3fbf73</cites><orcidid>0000-0003-3970-3144</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcb.26669$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.26669$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27929,27930,45579,45580</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29323744$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chang, Zong‐kun</creatorcontrib><creatorcontrib>Meng, Fan‐gang</creatorcontrib><creatorcontrib>Zhang, Zhi‐qi</creatorcontrib><creatorcontrib>Mao, Gu‐ping</creatorcontrib><creatorcontrib>Huang, Zhi‐yu</creatorcontrib><creatorcontrib>Liao, Wei‐ming</creatorcontrib><creatorcontrib>He, Ai‐shan</creatorcontrib><title>MicroRNA‐193b‐3p regulates matrix metalloproteinase 19 expression in interleukin‐1β‐induced human chondrocytes</title><title>Journal of cellular biochemistry</title><addtitle>J Cell Biochem</addtitle><description>Micro(mi)RNAs are small, non‐coding RNA molecules known to play a significant role in osteoarthritis (OA) initiation and development, and similar to matrix metalloproteinases (MMPs), they participate in cartilage degeneration and cleave multiple extracellular matrices. The aim of this study was to determine whether the expression of MMP‐19 in interleukin (IL)‐1β‐induced human chondrocytes is directly regulated by miR‐193b‐3p. Expression levels of miR‐193b‐3p and MMP‐19 in normal and osteoarthritis (OA) human cartilage, and interleukin‐1 β (IL‐1β)‐induced human chondrocytes were determined by real‐time polymerase chain reaction. Additionally, expression level of MMP‐19 in IL‐1β‐induced human chondrocytes was estimated by Western blotting and immunohistochemistry analyses. The effect of miR‐193b‐3p on MMP‐19 expression was evaluated using transient transfection of normal human chondrocytes with miR‐193b‐3p mimic or its antisense inhibitor (miR‐193b‐3p inhibitor), and siMMP‐19. The putative binding site of miR‐193b‐3p in the 3′‐untranslated region (UTR) of MMP‐19 mRNA was validated by luciferase reporter assay. miR‐193b‐3p expression was reduced in OA cartilage compared to that in normal chondrocytes, while the opposite was observed for MMP‐19. Upregulation of MMP‐19 expression was correlated with downregulation of miR‐193b‐3p in IL‐1β‐stimulated normal chondrocytes. Increase in miR‐193b‐3p levels was associated with silencing of MMP‐19. Overexpression of miR‐193b‐3p suppressed the activity of the reporter construct containing the 3′‐UTR of human MMP‐19 mRNA and inhibited the IL‐1β‐induced expression of MMP‐19 and iNOS in chondrocytes, while treatment with miR‐193b‐3p inhibitor enhanced MMP‐19 expression. MiR‐193b‐3p is an important regulator of MMP‐19 in human chondrocytes and may relieve the inflammatory response in OA.
This study investigated the relationship of miR‐193b‐3p and MMP‐19 in osteoarthritis cartilage, and determined that microRNA‐193b‐3p (miR‐193b‐3p) regulates MMP‐19 expression in IL‐1β‐stimulated normal chondrocytes directly.</description><subject>3' Untranslated regions</subject><subject>Addition polymerization</subject><subject>Antisense RNA</subject><subject>Arthritis</subject><subject>Binding sites</subject><subject>Biocompatibility</subject><subject>Biomedical materials</subject><subject>Cartilage</subject><subject>Cartilage diseases</subject><subject>Chondrocytes</subject><subject>Cytokines</subject><subject>Degeneration</subject><subject>Gene expression</subject><subject>IL-1β</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Inflammatory response</subject><subject>Inhibitors</subject><subject>Interleukins</subject><subject>Matrix metalloproteinase</subject><subject>Matrix metalloproteinases</subject><subject>Metalloproteinase</subject><subject>miRNA</subject><subject>miR‐193b‐3p</subject><subject>MMP‐19</subject><subject>mRNA</subject><subject>Nitric-oxide synthase</subject><subject>Osteoarthritis</subject><subject>Polymerase chain reaction</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Test systems</subject><subject>Transfection</subject><subject>Western blotting</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp1kctOFEEUhisGIwO64AVIJ2xg0VC3rupawkRRg5oYXVfqchpq6MtQ1Z1hdj6Cz8KD-BA-iTUOsiAxqZx_8-Wrk_MjdEDwKcGYni2cPaVCCPUCzQhWsuSC8x00w5LhkjJCd9FeSguMsVKMvkK7NAeTnM_Q6lNwcfj6-fz3j59EMZuDLYsI11NrRkhFZ8YY7osORtO2wzIOI4TeJCiIKuB-GSGlMPRF2LwRYgvTbeg3rl8PeYbeTw58cTN1pi_czdD7OLh1Fr9GLxvTJnjzmPvo-7u33-bvy6svlx_m51elYxVTpaSCemuFNw6qumLS14x7Yx23hjMluLHYYlrXihqQxvhG0Ya6RnpgjW0k20fHW29e_W6CNOouJAdta3oYpqSJqlUlRMVJRo-eoYthin3eTlNM819SVDhTJ1sqny2lCI1extCZuNYE600bOreh_7aR2cNH42Q78E_kv_Nn4GwLrEIL6_-b9Mf5xVb5B1k4md4</recordid><startdate>201806</startdate><enddate>201806</enddate><creator>Chang, Zong‐kun</creator><creator>Meng, Fan‐gang</creator><creator>Zhang, Zhi‐qi</creator><creator>Mao, Gu‐ping</creator><creator>Huang, Zhi‐yu</creator><creator>Liao, Wei‐ming</creator><creator>He, Ai‐shan</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-3970-3144</orcidid></search><sort><creationdate>201806</creationdate><title>MicroRNA‐193b‐3p regulates matrix metalloproteinase 19 expression in interleukin‐1β‐induced human chondrocytes</title><author>Chang, Zong‐kun ; Meng, Fan‐gang ; Zhang, Zhi‐qi ; Mao, Gu‐ping ; Huang, Zhi‐yu ; Liao, Wei‐ming ; He, Ai‐shan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3539-7262dbb6dace58537d834dabc4ba43964ab0b028892ae7aadf92f2cf7de3fbf73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>3' Untranslated regions</topic><topic>Addition polymerization</topic><topic>Antisense RNA</topic><topic>Arthritis</topic><topic>Binding sites</topic><topic>Biocompatibility</topic><topic>Biomedical materials</topic><topic>Cartilage</topic><topic>Cartilage diseases</topic><topic>Chondrocytes</topic><topic>Cytokines</topic><topic>Degeneration</topic><topic>Gene expression</topic><topic>IL-1β</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Inflammatory response</topic><topic>Inhibitors</topic><topic>Interleukins</topic><topic>Matrix metalloproteinase</topic><topic>Matrix metalloproteinases</topic><topic>Metalloproteinase</topic><topic>miRNA</topic><topic>miR‐193b‐3p</topic><topic>MMP‐19</topic><topic>mRNA</topic><topic>Nitric-oxide synthase</topic><topic>Osteoarthritis</topic><topic>Polymerase chain reaction</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>Test systems</topic><topic>Transfection</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chang, Zong‐kun</creatorcontrib><creatorcontrib>Meng, Fan‐gang</creatorcontrib><creatorcontrib>Zhang, Zhi‐qi</creatorcontrib><creatorcontrib>Mao, Gu‐ping</creatorcontrib><creatorcontrib>Huang, Zhi‐yu</creatorcontrib><creatorcontrib>Liao, Wei‐ming</creatorcontrib><creatorcontrib>He, Ai‐shan</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences 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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chang, Zong‐kun</au><au>Meng, Fan‐gang</au><au>Zhang, Zhi‐qi</au><au>Mao, Gu‐ping</au><au>Huang, Zhi‐yu</au><au>Liao, Wei‐ming</au><au>He, Ai‐shan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MicroRNA‐193b‐3p regulates matrix metalloproteinase 19 expression in interleukin‐1β‐induced human chondrocytes</atitle><jtitle>Journal of cellular biochemistry</jtitle><addtitle>J Cell Biochem</addtitle><date>2018-06</date><risdate>2018</risdate><volume>119</volume><issue>6</issue><spage>4775</spage><epage>4782</epage><pages>4775-4782</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><abstract>Micro(mi)RNAs are small, non‐coding RNA molecules known to play a significant role in osteoarthritis (OA) initiation and development, and similar to matrix metalloproteinases (MMPs), they participate in cartilage degeneration and cleave multiple extracellular matrices. The aim of this study was to determine whether the expression of MMP‐19 in interleukin (IL)‐1β‐induced human chondrocytes is directly regulated by miR‐193b‐3p. Expression levels of miR‐193b‐3p and MMP‐19 in normal and osteoarthritis (OA) human cartilage, and interleukin‐1 β (IL‐1β)‐induced human chondrocytes were determined by real‐time polymerase chain reaction. Additionally, expression level of MMP‐19 in IL‐1β‐induced human chondrocytes was estimated by Western blotting and immunohistochemistry analyses. The effect of miR‐193b‐3p on MMP‐19 expression was evaluated using transient transfection of normal human chondrocytes with miR‐193b‐3p mimic or its antisense inhibitor (miR‐193b‐3p inhibitor), and siMMP‐19. The putative binding site of miR‐193b‐3p in the 3′‐untranslated region (UTR) of MMP‐19 mRNA was validated by luciferase reporter assay. miR‐193b‐3p expression was reduced in OA cartilage compared to that in normal chondrocytes, while the opposite was observed for MMP‐19. Upregulation of MMP‐19 expression was correlated with downregulation of miR‐193b‐3p in IL‐1β‐stimulated normal chondrocytes. Increase in miR‐193b‐3p levels was associated with silencing of MMP‐19. Overexpression of miR‐193b‐3p suppressed the activity of the reporter construct containing the 3′‐UTR of human MMP‐19 mRNA and inhibited the IL‐1β‐induced expression of MMP‐19 and iNOS in chondrocytes, while treatment with miR‐193b‐3p inhibitor enhanced MMP‐19 expression. MiR‐193b‐3p is an important regulator of MMP‐19 in human chondrocytes and may relieve the inflammatory response in OA.
This study investigated the relationship of miR‐193b‐3p and MMP‐19 in osteoarthritis cartilage, and determined that microRNA‐193b‐3p (miR‐193b‐3p) regulates MMP‐19 expression in IL‐1β‐stimulated normal chondrocytes directly.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>29323744</pmid><doi>10.1002/jcb.26669</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0003-3970-3144</orcidid></addata></record> |
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subjects | 3' Untranslated regions Addition polymerization Antisense RNA Arthritis Binding sites Biocompatibility Biomedical materials Cartilage Cartilage diseases Chondrocytes Cytokines Degeneration Gene expression IL-1β Immunohistochemistry Inflammation Inflammatory response Inhibitors Interleukins Matrix metalloproteinase Matrix metalloproteinases Metalloproteinase miRNA miR‐193b‐3p MMP‐19 mRNA Nitric-oxide synthase Osteoarthritis Polymerase chain reaction Ribonucleic acid RNA Test systems Transfection Western blotting |
title | MicroRNA‐193b‐3p regulates matrix metalloproteinase 19 expression in interleukin‐1β‐induced human chondrocytes |
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