Effects of miR-150-5p on the growth and SOCS1 expression of rheumatoid arthritis synovial fibroblasts
Objective miR-150-5p has been implicated in the regulation and onset of immune diseases. We investigated the effects of miR-150-5p on the functions of RA synovial fibroblasts (RASFs). Method The binding site between suppressor of cytokine signaling 1 (SOCS1) and miR-150-5p was analyzed using Europea...
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creator | Qiu, Mingliang Mo, Lisha Li, Juxiang Liang, Hua Zhu, Weina Zheng, Xiangjuan Duan, Xinwang Xu, Weidong |
description | Objective
miR-150-5p has been implicated in the regulation and onset of immune diseases. We investigated the effects of miR-150-5p on the functions of RA synovial fibroblasts (RASFs).
Method
The binding site between suppressor of cytokine signaling 1 (SOCS1) and miR-150-5p was analyzed using European Bioinformatics Institute database, and the 3′ UTR of SOCS1 mRNA, including the binding site, was amplified and ligated to the 3′-end of LUC2 gene in the pmirGL0 dual-luciferase vector. The pmirGL0 vector and corresponding mimics were subsequently co-transfected into 293T cells to compare the relative fluorescence intensity of LUC2 between the miR-150-5p mimics and the negative control (NC) mimics groups. Further, the RASF cell line MH7A was transfected with miR-150-5p or NC mimics and subjected to flow cytometric analysis, cell counting kit-8 assay, western blot analysis, qPCR, and enzyme-linked immunosorbent (ELISA) assay 48 h after transfection.
Results
miR-150-5p mimics resulted in a lower cell apoptotic rate and proportion of cells in the S phase. Using a dual-luciferase reporter gene assay, we then found that SOCS1 is a potential target of miR-150-5p. Compared with NC mimics, miR-150-5p mimics significantly decreased the protein and mRNA expression levels of SOCS1. ELISA assay showed that miR-150-5p mimics increased interleukin-6 level in the cell culture medium but did not influence tumor necrosis factor-alpha levels.
Conclusions
Overall, the growth-promoting effect of miR-150-5p on MH7A cells may be attributed to the miR-150-5p-induced degradation of
SOCS1
mRNA, suggesting a potential therapeutic target for RA.
Key Points
•
SOCS1 is a potential target of miR-150-5p
.
•
miR-150-5p promoted the growth of RASF cell line MH7A
.
•
miR-150-5p increased the secretion of IL-6 but did not significantly affect TNF-α levels in MH7A cells
. |
doi_str_mv | 10.1007/s10067-019-04894-7 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2331257773</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2375666934</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-93e2f4a7d97590b7d5e6f0e574c1108c02d306be769fdb3e6cf23365df2ca3d93</originalsourceid><addsrcrecordid>eNp9kUFP3DAQhS0EKlvgD3CoLHHpxcWOYzs-ohUtlZCQoD1bTjxmjZJ4sR1a_n0NS1uph15mDvO9N6N5CJ0y-olRqs5zrVIRyjShbadbovbQirW8JVq3eh-tqFKUcKa7Q_Q-5wdKadNp9g4dctYp3Qm9QnDpPQwl4-jxFG4JE5SILY4zLhvA9yn-KBtsZ4fvbtZ3DMPPbYKcQ51XQdrAMtkSg8M2lU0KJWScn-f4FOyIfehT7EebSz5GB96OGU7e-hH6_vny2_qKXN98-bq-uCYDV6IQzaHxrVVOK6Fpr5wA6SkI1Q6M0W6gjeNU9qCk9q7nIAffcC6F881gudP8CH3c-W5TfFwgFzOFPMA42hnikk2lWSOUUryiZ_-gD3FJc72uUkpIKTVvK9XsqCHFnBN4s01hsunZMGpeQjC7EEwNwbyGYFQVfXizXvoJ3B_J769XgO-AXEfzPaS_u_9j-wtSupFj</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2375666934</pqid></control><display><type>article</type><title>Effects of miR-150-5p on the growth and SOCS1 expression of rheumatoid arthritis synovial fibroblasts</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Qiu, Mingliang ; Mo, Lisha ; Li, Juxiang ; Liang, Hua ; Zhu, Weina ; Zheng, Xiangjuan ; Duan, Xinwang ; Xu, Weidong</creator><creatorcontrib>Qiu, Mingliang ; Mo, Lisha ; Li, Juxiang ; Liang, Hua ; Zhu, Weina ; Zheng, Xiangjuan ; Duan, Xinwang ; Xu, Weidong</creatorcontrib><description>Objective
miR-150-5p has been implicated in the regulation and onset of immune diseases. We investigated the effects of miR-150-5p on the functions of RA synovial fibroblasts (RASFs).
Method
The binding site between suppressor of cytokine signaling 1 (SOCS1) and miR-150-5p was analyzed using European Bioinformatics Institute database, and the 3′ UTR of SOCS1 mRNA, including the binding site, was amplified and ligated to the 3′-end of LUC2 gene in the pmirGL0 dual-luciferase vector. The pmirGL0 vector and corresponding mimics were subsequently co-transfected into 293T cells to compare the relative fluorescence intensity of LUC2 between the miR-150-5p mimics and the negative control (NC) mimics groups. Further, the RASF cell line MH7A was transfected with miR-150-5p or NC mimics and subjected to flow cytometric analysis, cell counting kit-8 assay, western blot analysis, qPCR, and enzyme-linked immunosorbent (ELISA) assay 48 h after transfection.
Results
miR-150-5p mimics resulted in a lower cell apoptotic rate and proportion of cells in the S phase. Using a dual-luciferase reporter gene assay, we then found that SOCS1 is a potential target of miR-150-5p. Compared with NC mimics, miR-150-5p mimics significantly decreased the protein and mRNA expression levels of SOCS1. ELISA assay showed that miR-150-5p mimics increased interleukin-6 level in the cell culture medium but did not influence tumor necrosis factor-alpha levels.
Conclusions
Overall, the growth-promoting effect of miR-150-5p on MH7A cells may be attributed to the miR-150-5p-induced degradation of
SOCS1
mRNA, suggesting a potential therapeutic target for RA.
Key Points
•
SOCS1 is a potential target of miR-150-5p
.
•
miR-150-5p promoted the growth of RASF cell line MH7A
.
•
miR-150-5p increased the secretion of IL-6 but did not significantly affect TNF-α levels in MH7A cells
.</description><identifier>ISSN: 0770-3198</identifier><identifier>EISSN: 1434-9949</identifier><identifier>DOI: 10.1007/s10067-019-04894-7</identifier><identifier>PMID: 31879859</identifier><language>eng</language><publisher>London: Springer London</publisher><subject>3' Untranslated Regions ; Apoptosis ; Arthritis, Rheumatoid - genetics ; Arthritis, Rheumatoid - metabolism ; Arthritis, Rheumatoid - pathology ; Binding sites ; Bioinformatics ; Cell culture ; Cell Line ; Cell Proliferation ; Cells, Cultured ; Enzyme-linked immunosorbent assay ; Fibroblasts ; Fibroblasts - metabolism ; Fibroblasts - pathology ; Flow cytometry ; Gene expression ; Humans ; Immunological diseases ; Interleukin 6 ; Interleukin-6 - metabolism ; Medicine ; Medicine & Public Health ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Original Article ; Reporter gene ; Rheumatoid arthritis ; Rheumatology ; RNA, Messenger - metabolism ; S phase ; SOCS-1 protein ; Suppressor of Cytokine Signaling 1 Protein - genetics ; Suppressor of Cytokine Signaling 1 Protein - metabolism ; Synovial Membrane - metabolism ; Synovial Membrane - pathology ; Therapeutic applications ; Transfection ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α</subject><ispartof>Clinical rheumatology, 2020-03, Vol.39 (3), p.909-917</ispartof><rights>International League of Associations for Rheumatology (ILAR) 2019. corrected publication 2020</rights><rights>Clinical Rheumatology is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-93e2f4a7d97590b7d5e6f0e574c1108c02d306be769fdb3e6cf23365df2ca3d93</citedby><cites>FETCH-LOGICAL-c375t-93e2f4a7d97590b7d5e6f0e574c1108c02d306be769fdb3e6cf23365df2ca3d93</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/s10067-019-04894-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10067-019-04894-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27922,27923,41486,42555,51317</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31879859$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qiu, Mingliang</creatorcontrib><creatorcontrib>Mo, Lisha</creatorcontrib><creatorcontrib>Li, Juxiang</creatorcontrib><creatorcontrib>Liang, Hua</creatorcontrib><creatorcontrib>Zhu, Weina</creatorcontrib><creatorcontrib>Zheng, Xiangjuan</creatorcontrib><creatorcontrib>Duan, Xinwang</creatorcontrib><creatorcontrib>Xu, Weidong</creatorcontrib><title>Effects of miR-150-5p on the growth and SOCS1 expression of rheumatoid arthritis synovial fibroblasts</title><title>Clinical rheumatology</title><addtitle>Clin Rheumatol</addtitle><addtitle>Clin Rheumatol</addtitle><description>Objective
miR-150-5p has been implicated in the regulation and onset of immune diseases. We investigated the effects of miR-150-5p on the functions of RA synovial fibroblasts (RASFs).
Method
The binding site between suppressor of cytokine signaling 1 (SOCS1) and miR-150-5p was analyzed using European Bioinformatics Institute database, and the 3′ UTR of SOCS1 mRNA, including the binding site, was amplified and ligated to the 3′-end of LUC2 gene in the pmirGL0 dual-luciferase vector. The pmirGL0 vector and corresponding mimics were subsequently co-transfected into 293T cells to compare the relative fluorescence intensity of LUC2 between the miR-150-5p mimics and the negative control (NC) mimics groups. Further, the RASF cell line MH7A was transfected with miR-150-5p or NC mimics and subjected to flow cytometric analysis, cell counting kit-8 assay, western blot analysis, qPCR, and enzyme-linked immunosorbent (ELISA) assay 48 h after transfection.
Results
miR-150-5p mimics resulted in a lower cell apoptotic rate and proportion of cells in the S phase. Using a dual-luciferase reporter gene assay, we then found that SOCS1 is a potential target of miR-150-5p. Compared with NC mimics, miR-150-5p mimics significantly decreased the protein and mRNA expression levels of SOCS1. ELISA assay showed that miR-150-5p mimics increased interleukin-6 level in the cell culture medium but did not influence tumor necrosis factor-alpha levels.
Conclusions
Overall, the growth-promoting effect of miR-150-5p on MH7A cells may be attributed to the miR-150-5p-induced degradation of
SOCS1
mRNA, suggesting a potential therapeutic target for RA.
Key Points
•
SOCS1 is a potential target of miR-150-5p
.
•
miR-150-5p promoted the growth of RASF cell line MH7A
.
•
miR-150-5p increased the secretion of IL-6 but did not significantly affect TNF-α levels in MH7A cells
.</description><subject>3' Untranslated Regions</subject><subject>Apoptosis</subject><subject>Arthritis, Rheumatoid - genetics</subject><subject>Arthritis, Rheumatoid - metabolism</subject><subject>Arthritis, Rheumatoid - pathology</subject><subject>Binding sites</subject><subject>Bioinformatics</subject><subject>Cell culture</subject><subject>Cell Line</subject><subject>Cell Proliferation</subject><subject>Cells, Cultured</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Fibroblasts</subject><subject>Fibroblasts - metabolism</subject><subject>Fibroblasts - pathology</subject><subject>Flow cytometry</subject><subject>Gene expression</subject><subject>Humans</subject><subject>Immunological diseases</subject><subject>Interleukin 6</subject><subject>Interleukin-6 - metabolism</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Original Article</subject><subject>Reporter gene</subject><subject>Rheumatoid arthritis</subject><subject>Rheumatology</subject><subject>RNA, Messenger - metabolism</subject><subject>S phase</subject><subject>SOCS-1 protein</subject><subject>Suppressor of Cytokine Signaling 1 Protein - genetics</subject><subject>Suppressor of Cytokine Signaling 1 Protein - metabolism</subject><subject>Synovial Membrane - metabolism</subject><subject>Synovial Membrane - pathology</subject><subject>Therapeutic applications</subject><subject>Transfection</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><issn>0770-3198</issn><issn>1434-9949</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kUFP3DAQhS0EKlvgD3CoLHHpxcWOYzs-ohUtlZCQoD1bTjxmjZJ4sR1a_n0NS1uph15mDvO9N6N5CJ0y-olRqs5zrVIRyjShbadbovbQirW8JVq3eh-tqFKUcKa7Q_Q-5wdKadNp9g4dctYp3Qm9QnDpPQwl4-jxFG4JE5SILY4zLhvA9yn-KBtsZ4fvbtZ3DMPPbYKcQ51XQdrAMtkSg8M2lU0KJWScn-f4FOyIfehT7EebSz5GB96OGU7e-hH6_vny2_qKXN98-bq-uCYDV6IQzaHxrVVOK6Fpr5wA6SkI1Q6M0W6gjeNU9qCk9q7nIAffcC6F881gudP8CH3c-W5TfFwgFzOFPMA42hnikk2lWSOUUryiZ_-gD3FJc72uUkpIKTVvK9XsqCHFnBN4s01hsunZMGpeQjC7EEwNwbyGYFQVfXizXvoJ3B_J769XgO-AXEfzPaS_u_9j-wtSupFj</recordid><startdate>20200301</startdate><enddate>20200301</enddate><creator>Qiu, Mingliang</creator><creator>Mo, Lisha</creator><creator>Li, Juxiang</creator><creator>Liang, Hua</creator><creator>Zhu, Weina</creator><creator>Zheng, Xiangjuan</creator><creator>Duan, Xinwang</creator><creator>Xu, Weidong</creator><general>Springer London</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>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>7X8</scope></search><sort><creationdate>20200301</creationdate><title>Effects of miR-150-5p on the growth and SOCS1 expression of rheumatoid arthritis synovial fibroblasts</title><author>Qiu, Mingliang ; Mo, Lisha ; Li, Juxiang ; Liang, Hua ; Zhu, Weina ; Zheng, Xiangjuan ; Duan, Xinwang ; Xu, Weidong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-93e2f4a7d97590b7d5e6f0e574c1108c02d306be769fdb3e6cf23365df2ca3d93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>3' Untranslated Regions</topic><topic>Apoptosis</topic><topic>Arthritis, Rheumatoid - genetics</topic><topic>Arthritis, Rheumatoid - metabolism</topic><topic>Arthritis, Rheumatoid - pathology</topic><topic>Binding sites</topic><topic>Bioinformatics</topic><topic>Cell culture</topic><topic>Cell Line</topic><topic>Cell Proliferation</topic><topic>Cells, Cultured</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Fibroblasts</topic><topic>Fibroblasts - metabolism</topic><topic>Fibroblasts - pathology</topic><topic>Flow cytometry</topic><topic>Gene expression</topic><topic>Humans</topic><topic>Immunological diseases</topic><topic>Interleukin 6</topic><topic>Interleukin-6 - metabolism</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Original Article</topic><topic>Reporter gene</topic><topic>Rheumatoid arthritis</topic><topic>Rheumatology</topic><topic>RNA, Messenger - metabolism</topic><topic>S phase</topic><topic>SOCS-1 protein</topic><topic>Suppressor of Cytokine Signaling 1 Protein - genetics</topic><topic>Suppressor of Cytokine Signaling 1 Protein - metabolism</topic><topic>Synovial Membrane - metabolism</topic><topic>Synovial Membrane - pathology</topic><topic>Therapeutic applications</topic><topic>Transfection</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Qiu, Mingliang</creatorcontrib><creatorcontrib>Mo, Lisha</creatorcontrib><creatorcontrib>Li, Juxiang</creatorcontrib><creatorcontrib>Liang, Hua</creatorcontrib><creatorcontrib>Zhu, Weina</creatorcontrib><creatorcontrib>Zheng, Xiangjuan</creatorcontrib><creatorcontrib>Duan, Xinwang</creatorcontrib><creatorcontrib>Xu, Weidong</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>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>MEDLINE - Academic</collection><jtitle>Clinical rheumatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Qiu, Mingliang</au><au>Mo, Lisha</au><au>Li, Juxiang</au><au>Liang, Hua</au><au>Zhu, Weina</au><au>Zheng, Xiangjuan</au><au>Duan, Xinwang</au><au>Xu, Weidong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of miR-150-5p on the growth and SOCS1 expression of rheumatoid arthritis synovial fibroblasts</atitle><jtitle>Clinical rheumatology</jtitle><stitle>Clin Rheumatol</stitle><addtitle>Clin Rheumatol</addtitle><date>2020-03-01</date><risdate>2020</risdate><volume>39</volume><issue>3</issue><spage>909</spage><epage>917</epage><pages>909-917</pages><issn>0770-3198</issn><eissn>1434-9949</eissn><abstract>Objective
miR-150-5p has been implicated in the regulation and onset of immune diseases. We investigated the effects of miR-150-5p on the functions of RA synovial fibroblasts (RASFs).
Method
The binding site between suppressor of cytokine signaling 1 (SOCS1) and miR-150-5p was analyzed using European Bioinformatics Institute database, and the 3′ UTR of SOCS1 mRNA, including the binding site, was amplified and ligated to the 3′-end of LUC2 gene in the pmirGL0 dual-luciferase vector. The pmirGL0 vector and corresponding mimics were subsequently co-transfected into 293T cells to compare the relative fluorescence intensity of LUC2 between the miR-150-5p mimics and the negative control (NC) mimics groups. Further, the RASF cell line MH7A was transfected with miR-150-5p or NC mimics and subjected to flow cytometric analysis, cell counting kit-8 assay, western blot analysis, qPCR, and enzyme-linked immunosorbent (ELISA) assay 48 h after transfection.
Results
miR-150-5p mimics resulted in a lower cell apoptotic rate and proportion of cells in the S phase. Using a dual-luciferase reporter gene assay, we then found that SOCS1 is a potential target of miR-150-5p. Compared with NC mimics, miR-150-5p mimics significantly decreased the protein and mRNA expression levels of SOCS1. ELISA assay showed that miR-150-5p mimics increased interleukin-6 level in the cell culture medium but did not influence tumor necrosis factor-alpha levels.
Conclusions
Overall, the growth-promoting effect of miR-150-5p on MH7A cells may be attributed to the miR-150-5p-induced degradation of
SOCS1
mRNA, suggesting a potential therapeutic target for RA.
Key Points
•
SOCS1 is a potential target of miR-150-5p
.
•
miR-150-5p promoted the growth of RASF cell line MH7A
.
•
miR-150-5p increased the secretion of IL-6 but did not significantly affect TNF-α levels in MH7A cells
.</abstract><cop>London</cop><pub>Springer London</pub><pmid>31879859</pmid><doi>10.1007/s10067-019-04894-7</doi><tpages>9</tpages></addata></record> |
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subjects | 3' Untranslated Regions Apoptosis Arthritis, Rheumatoid - genetics Arthritis, Rheumatoid - metabolism Arthritis, Rheumatoid - pathology Binding sites Bioinformatics Cell culture Cell Line Cell Proliferation Cells, Cultured Enzyme-linked immunosorbent assay Fibroblasts Fibroblasts - metabolism Fibroblasts - pathology Flow cytometry Gene expression Humans Immunological diseases Interleukin 6 Interleukin-6 - metabolism Medicine Medicine & Public Health MicroRNAs - genetics MicroRNAs - metabolism Original Article Reporter gene Rheumatoid arthritis Rheumatology RNA, Messenger - metabolism S phase SOCS-1 protein Suppressor of Cytokine Signaling 1 Protein - genetics Suppressor of Cytokine Signaling 1 Protein - metabolism Synovial Membrane - metabolism Synovial Membrane - pathology Therapeutic applications Transfection Tumor necrosis factor-TNF Tumor necrosis factor-α |
title | Effects of miR-150-5p on the growth and SOCS1 expression of rheumatoid arthritis synovial fibroblasts |
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