Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 조성신 | - |
dc.date.accessioned | 2019-12-10T16:36:02Z | - |
dc.date.available | 2019-12-10T16:36:02Z | - |
dc.date.issued | 2018-12 | - |
dc.identifier.citation | IMMUNOLOGY LETTERS, v. 206, page. 33-40 | en_US |
dc.identifier.issn | 0165-2478 | - |
dc.identifier.issn | 1879-0542 | - |
dc.identifier.uri | https://www.sciencedirect.com/science/article/abs/pii/S0165247818304206?via%3Dihub | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/121039 | - |
dc.description.abstract | TGF-beta 1 is highly expressed in the synovial tissue of patients with rheumatoid arthritis and is known as a cytokine that plays an important role in tissue repair and immune cell regulation. However, the role of TGF-beta 1 is still unclear in osteoclastogenesis. In this study, we examined the effect of TGF-beta 11 on osteoclast differentiation and the underlying mechanism using healthy human peripheral blood monocytes. TGF-beta 1 was found to inhibit osteoclast differentiation and decrease the expression of osteoclast-specific genes such as acid phosphatase 5, tartrate resistant and cathepsin K. Levels of NFAT1, an important transcription factor in osteoclastogenesis, were also reduced. In addition, TGF-beta 11 suppressed receptor activator of NF-x13 (RANK) ligand-induced NF-kappa B and p38 MAPK signaling. Inhibition of osteoclast differentiation by TGF-beta 1 was reversed by 1 pM SB431542 (an inhibitor of ALK4/5/7), which inhibited TGF-beta 1-induced phosphorylation of SMAD1, but not that of SMAD3. TGF-beta 1 also restricted RANK expression, and this was partially reversed by 1 pM SB431542. In contrast, the inhibition of SMAD3 by SIS3 (an inhibitor of SMAD3) reduced the osteoclast formation. TGF-f31 has both inhibitory and stimulatory effects on human osteoclast differentiation, and that these opposing functions are mediated by SMAD1 and SMAD3 signaling, respectively. | en_US |
dc.description.sponsorship | This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2017R 1D 1A 1B03028389 to Jong Dae Ji) and the Ministry of Science, ICT, & Future (NRF-2016R1A2B4008606), and a grant of the Korea Health Technology R&D project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (HI17C0888). | en_US |
dc.language.iso | en_US | en_US |
dc.publisher | ELSEVIER SCIENCE BV | en_US |
dc.subject | Osteoclast | en_US |
dc.subject | TGF-beta | en_US |
dc.subject | Smad1 | en_US |
dc.subject | Smad3 | en_US |
dc.title | A dual role of TGF-β in human osteoclast differentiation mediated by Smad1 versus Smad3 signaling. | en_US |
dc.type | Article | en_US |
dc.identifier.doi | 10.1016/j.imlet.2018.12.003 | - |
dc.relation.page | 33-40 | - |
dc.relation.journal | IMMUNOLOGY LETTERS | - |
dc.contributor.googleauthor | Lee, Bitnara | - |
dc.contributor.googleauthor | Oh, Younseo | - |
dc.contributor.googleauthor | Jo, Sungsin | - |
dc.contributor.googleauthor | Kim, Tae-Hwan | - |
dc.contributor.googleauthor | Ji, Jong Dae | - |
dc.relation.code | 2018012373 | - |
dc.sector.campus | S | - |
dc.sector.daehak | RESEARCH INSTITUTE[S] | - |
dc.sector.department | RHEUMATISM CENTER | - |
dc.identifier.pid | joejo0517 | - |
dc.identifier.orcid | http://orcid.org/0000-0003-3034-5029 | - |
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