PMID- 31239367 OWN - NLM STAT- MEDLINE DCOM- 20200911 LR - 20200911 IS - 1573-4935 (Electronic) IS - 0144-8463 (Print) IS - 0144-8463 (Linking) VI - 39 IP - 7 DP - 2019 Jul 31 TI - Down-regulation of microRNA-142-3p inhibits the aggressive phenotypes of rheumatoid arthritis fibroblast-like synoviocytes through inhibiting nuclear factor-kappaB signaling. LID - BSR20190700 [pii] LID - 10.1042/BSR20190700 [doi] AB - The present study aimed to investigate the regulatory roles of miR-142-3p on the aggressive phenotypes of rheumatoid arthritis (RA) human fibroblast-like synoviocytes (RA-HFLSs), and reveal the potential mechanisms relating with nuclear factor-kappaB (NF-kappaB) signaling. miR-142-3p expression was detected in RA synovial tissues and RA-HFLSs by quantitative real-time PCR (qRT-PCR) and Northern blot analysis. RA-HFLSs were transfected with miR-142-3p inhibitor and/or treated with 10 microg/l tumor necrosis factor alpha (TNF-alpha). The viability, colony formation, apoptosis, migration, invasion, and the levels of interleukin (IL)-6, and matrix metalloproteinase 3 (MMP-3) were detected. The mRNA expressions of B-cell lymphoma-2 (Bcl-2), Bax, Bad, IL-6, and MMP-3 were detected by qRT-PCR. Moreover, the expression of Bcl-2, IL-1 receptor-associated kinase 1 (IRAK1), Toll-like receptor 4 (TLR4), NF-kappaB p65, and phosphorylated NF-kappaB p65 (p-NF-kappaB p65) were detected by Western blot. The interaction between IRAK1 and miR-142-3p was identified by dual luciferase reporter gene assay. MiR-142-3p was up-regulated in RA synovial tissues and RA-HFLSs. TNF-alpha activated the aggressive phenotypes of RA-HFLSs, including enhanced proliferation, migration, invasion, and inflammation, and inhibited apoptosis. miR-142-3p inhibitor significantly decreased the cell viability, the number of cell clones, the migration rate, the number of invasive cells, the contents and expression of IL-6 and MMP-3, and increased the apoptosis rate and the expressions of Bax and Bad, and decreased Bcl-2 expression of TNF-alpha-treated RA-HFLSs. MiR-142-3p inhibitor significantly reversed TNF-alpha-induced up-regulation of IRAK1, TLR4, and p-NF-kappaB p65 in TNF-alpha-treated RA-HFLSs. Besides, IRAK1 was a target of miR-142-3p. The down-regulation of miR-142-3p inhibited the aggressive phenotypes of RA-HFLSs through inhibiting NF-kappaB signaling. CI - (c) 2019 The Author(s). FAU - Qiang, Jianhong AU - Qiang J AD - Department of Traditional Chinese Medicine, Yan'An People's Hospital, No. 57, Qilipu Street, Baota District, Yan'an City 716000, Shaanxi Province, China. FAU - Lv, Tingting AU - Lv T AD - Department of Rheumatology and Immunology, The Second Affiliated Hospital of The Fourth Military Medical University, No. 569, Xinsi Road, Xi'an City 710038, Shaanxi Province, China. FAU - Wu, Zhenbiao AU - Wu Z AD - Department of Clinical Immunology, The First Affiliated Hospital of The Fourth Military Medical University, No. 1, Changle East Road, Xi'an City 710032, Shaanxi Province, China. FAU - Yang, Xichao AU - Yang X AUID- ORCID: 0000-0001-9187-8457 AD - Department of Clinical Immunology, The First Affiliated Hospital of The Fourth Military Medical University, No. 1, Changle East Road, Xi'an City 710032, Shaanxi Province, China yangxichao258@163.com. LA - eng PT - Journal Article PT - Retracted Publication DEP - 20190708 PL - England TA - Biosci Rep JT - Bioscience reports JID - 8102797 RN - 0 (MIRN142 microRNA, human) RN - 0 (MicroRNAs) RN - 0 (NF-kappa B) RN - 0 (Tumor Necrosis Factor-alpha) RN - EC 2.7.11.1 (IRAK1 protein, human) RN - EC 2.7.11.1 (Interleukin-1 Receptor-Associated Kinases) RN - EC 3.4.24.17 (MMP3 protein, human) RN - EC 3.4.24.17 (Matrix Metalloproteinase 3) SB - IM ECI - Biosci Rep. 2020 Jun 26;40(6):. PMID: 32584394 RIN - Biosci Rep. 2020 Sep 30;40(9):. PMID: 32869853 MH - Arthritis, Rheumatoid/*genetics/pathology MH - Cell Proliferation/genetics MH - Female MH - Fibroblasts/metabolism/pathology MH - Gene Expression Regulation/genetics MH - Humans MH - Inflammation/genetics/pathology MH - Interleukin-1 Receptor-Associated Kinases/*genetics MH - Male MH - Matrix Metalloproteinase 3/genetics MH - MicroRNAs/*genetics MH - Middle Aged MH - NF-kappa B/*genetics MH - Signal Transduction/genetics MH - Synovial Membrane/metabolism/pathology MH - Synoviocytes/metabolism/pathology MH - Tumor Necrosis Factor-alpha/genetics PMC - PMC6614573 OTO - NOTNLM OT - Inflammation OT - MicroRNA-142-3p OT - Nuclear factor-kappa B OT - Proliferation OT - Tumor necrosis factor alpha COIS- The present study was conducted after obtaining approval of The First Affiliated Hospital of The Fourth Military Medical University's ethical committee. The research has been carried out in accordance with the World Medical Association Declaration of Helsinki, and that all subjects have been provided written informed consent. The authors declare that there are no competing interests associated with the manuscript. EDAT- 2019/06/27 06:00 MHDA- 2020/09/12 06:00 PMCR- 2019/07/08 CRDT- 2019/06/27 06:00 PHST- 2019/03/21 00:00 [received] PHST- 2019/06/16 00:00 [revised] PHST- 2019/06/19 00:00 [accepted] PHST- 2019/06/27 06:00 [pubmed] PHST- 2020/09/12 06:00 [medline] PHST- 2019/06/27 06:00 [entrez] PHST- 2019/07/08 00:00 [pmc-release] AID - BSR20190700 [pii] AID - 10.1042/BSR20190700 [doi] PST - epublish SO - Biosci Rep. 2019 Jul 8;39(7):BSR20190700. doi: 10.1042/BSR20190700. Print 2019 Jul 31.