| Project/Area Number |
15K09536
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Collagenous pathology/Allergology
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| Research Institution | Kyoto University |
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Principal Investigator |
TANAKA MASAO 京都大学, 医学研究科, 特定准教授 (10332719)
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| Co-Investigator(Kenkyū-buntansha) |
山本 靖彦 金沢大学, 医学系, 教授 (20313637)
杉本 直俊 金沢大学, 医学系, 准教授 (80272954)
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| Co-Investigator(Renkei-kenkyūsha) |
KIYOKAWA Etsuko 金沢医科大学, 医学部, 教授 (80300929)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 上皮間葉移行 / 関節滑膜細胞 / 関節リウマチ / DIP2A / SNAIL1 / EMT / DMAP結合ドメイン |
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| Outline of Final Research Achievements |
Our previous studies revealed that FSTL1 is one of the autoantigens in rheumatoid arthritis and DIP2A is its binding partner. In this study, we demonstrated molecular interaction between DIP2A and SNAI1, which is involved in epithelial-mesenchymal transition. Next, we analyzed synovial gene expression microarray data in US NCBI GEO database, which were from 79 subjects of three groups comprising rheumatoid arthritis, osteoarthritis patients and healthy controls. As a result, we found 9 gene groups in each of which genes had closely-related expression and those group genes had significantly different expression among the three groups. They include DIP2C and SNAI2, which are paralogs of DIP2A and SNAI1. Though DIP2C and SNAI2 belonged to the same groups as NFKB1 and TGFB1, respectively, they had inverted expression to those same members and similar behavior. As this contradicts the fact that TGFB1 induces SNAI1/2, there may be some dysregulation in rheumatoid synovium.
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