2016 Fiscal Year Final Research Report
Role of Endoplasmic reticulum stress response in rheumatoid arthritis
Project/Area Number |
15K20001
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Orthopaedic surgery
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Research Institution | Hiroshima University |
Principal Investigator |
Kanemoto Soshi 広島大学, 医歯薬保健学研究院(医), 講師 (90611913)
|
Project Period (FY) |
2015-04-01 – 2017-03-31
|
Keywords | 関節リウマチ / 小胞体ストレス / 破骨細胞 / 樹状細胞 / 小胞体膜局在転写因子 |
Outline of Final Research Achievements |
It has been reported that dysfunction of osteoclasts and dendritic cells occurs in rheumatoid arthritis(RA). However, it remains unclear whether function of endoplasmic reticulum (ER) in osteoclasts and dendritic cells is involved in pathogenesis of RA. In this study, analysis of mouse model for RA using conditional knockout mouse of ER-resident transcription factor Luman has been performed. Although in vivo investigation by RA mouse model was not able to obtain a concrete answer, in vitro investigation has revealed that Luman deficient dendritic cells attenuate the antigen-presenting ability, compared with wild type dendritic cells.
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Free Research Field |
生化学
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