Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 유대현 | - |
dc.date.accessioned | 2018-02-12T08:13:27Z | - |
dc.date.available | 2018-02-12T08:13:27Z | - |
dc.date.issued | 2011-10 | - |
dc.identifier.citation | JOINT BONE SPINE, 78 (5), 471-477 | en_US |
dc.identifier.issn | 1297-319X | - |
dc.identifier.uri | http://www.sciencedirect.com/science/article/pii/S1297319X11000054?_rdoc=1&_fmt=high&_origin=gateway&_docanchor=&md5=b8429449ccfc9c30159a5f9aeaa92ffb | - |
dc.description.abstract | Objective: Resistance to apoptosis of fibroblast-like synoviocytes (FLS) is considered as a major characteristic in RA. This study was designed to identify whether melittin has a pro-apoptotic effect in IL-6/sIL6R-stimulated human FLS by investigating the expression of mitochondrial apoptosis-related genes, nuclear factor-kappa B (NF-kappa B), and signal transducer and activators of transcription (STAT) activation.Methods: Cell viability was determined using a MTT assay after melittin treatment. Expressions of STAT3 and mitochondrial apoptosis-related genes induced by the IL-6/sIL-6R complex were determined by real time-polymerase chain reaction and western blotting. The expression of NF-kappa B p65 following IL-6 stimulation was determined by western blot analysis. The effects of melittin on the expression of apoptosis-related genes and the transcription factors NF-kappa B p65 and STAT3 were assessed in FLS. Apoptosis of FLS was determined by TUNEL-labeling to detect DNA strand breaks and DNA fragmentation assays. Caspase-3 activity was determined by a colorimetric assay.Results: IL-6/sIL-6R induced the activation of the transcription factors, STAT3, NF-kappa B p65 (nucleus), and Bcl-2. Melittin increased the expression of pro-apoptosis-related molecules, namely caspase-3, caspase-9, Apaf-1, and cytosolic cytochrome c, in a dose-dependent manner after treatment with IL-6/sIL-6R. Melittin inhibited STAT3 activation, translocation of NF-kappa B p65 into the nucleus, and expression of anti-apoptotic genes such as Bcl-2 and mitochondrial cytochrome c.Conclusions: The pro-apoptotic effects of melittin likely result from inhibition of the activation of the transcription factors, STAT3 and NF-kappa B p65, and regulation of mitochondrial apoptosis-related genes. Melittin is thus a promising therapeutic option for RA as it induces apoptosis in apoptosis-resistant synoviocytes. (C) 2011 Societe francaise de rhumatologie. Published by Elsevier Masson SAS. All rights reserved. | en_US |
dc.description.sponsorship | This work was supported by a grant (Code# 20070301034001) from the BioGreen 21 Program, Rural Development Administration, Republic of Korea. | en_US |
dc.language.iso | en | en_US |
dc.publisher | ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER, 23 RUE LINOIS, 75724 PARIS, FRANCE | en_US |
dc.subject | Melittin | en_US |
dc.subject | Synoviocyte | en_US |
dc.subject | Apoptosis | en_US |
dc.subject | STAT3 | en_US |
dc.subject | NF-kappa B | en_US |
dc.subject | IL-6 | en_US |
dc.subject | COLLAGEN-INDUCED ARTHRITIS | en_US |
dc.subject | BEE VENOM | en_US |
dc.subject | SYNOVIAL FIBROBLASTS | en_US |
dc.subject | MEDIATOR GENERATION | en_US |
dc.subject | JOINT DESTRUCTION | en_US |
dc.subject | CONTROLLED-TRIAL | en_US |
dc.subject | IL-6 RECEPTOR | en_US |
dc.subject | INTERLEUKIN-6 | en_US |
dc.subject | CELLS | en_US |
dc.subject | INFLAMMATION | en_US |
dc.title | Melittin enhances apoptosis through suppression of IL-6/sIL-6R complex-induced NF-kappa B and STAT3 activation and Bcl-2 expression for human fibroblast-like synoviocytes in rheumatoid arthritis | en_US |
dc.title.alternative | sIL-6R complex-induced NF-kappa B and STAT3 activation and Bcl-2 expression for human fibroblast-like synoviocytes in rheumatoid arthritis | en_US |
dc.type | Article | en_US |
dc.relation.no | 5 | - |
dc.relation.volume | 78 | - |
dc.identifier.doi | 10.1016/j.jbspin.2011.01.004 | - |
dc.relation.page | 471-477 | - |
dc.relation.journal | JOINT BONE SPINE | - |
dc.contributor.googleauthor | Kim, Seong-Kyu | - |
dc.contributor.googleauthor | Yoon, Wern-Chan | - |
dc.contributor.googleauthor | Park, Sung-Hoon | - |
dc.contributor.googleauthor | Choe, Jung-Yoon | - |
dc.contributor.googleauthor | Park, Ki-Yeun | - |
dc.contributor.googleauthor | Park, Kwan-Kyu | - |
dc.contributor.googleauthor | Yoo, Dae-Hyun | - |
dc.relation.code | 2011204537 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | dhyoo | - |
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