Inhibitory effects of H-Ras/Raf-1-binding affibody molecules on synovial cell function
| Project/Area Number |
24791013
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
膠原病・アレルギー・感染症内科学
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| Research Institution | Hyogo Medical University |
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Principal Investigator |
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| Research Collaborator |
IWASAKI Tsuyoshi 兵庫医療大学, 薬学部, 教授 (10151721)
SANO Hajime 兵庫医科大学, 医学部, 教授 (00196304)
SHIBASAKI Seiji 兵庫医療大学, 共通教育センター, 准教授 (50342530)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 人工抗体 / Affibody |
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| Outline of Final Research Achievements |
Affibody molecules targeting H-Ras (Zras122,Zras220, and Zras521) or Raf-1 (Zraf322) were introduced into the MH7A synovial cell line using two delivery methods: transfection with plasmids encoding the affibody molecules or direct introduction of affibody protein using a cell-penetrating peptide reagent. Affibody molecules could inhibit IL-6 and PGE2 production in TNF-α-stimulated MH7A cells. The inhibitory effect was stronger when affibody molecules were delivered as proteins via a cell-penetrating peptide reagent than when plasmid-DNA encoding the affibody moelcules was transfected into the cells. Plasmid-expressed Zras220 inhibited phosphorylation of ERK in TNF-α-stimulated MH7A cells. Protein-introduced Zraf322 inhibited the production of IL-6 and PGE2 and inhibited cell proliferation in MH7A cells. Affibody molecules specific for H-Ras and Raf-1 can affect intracellular signal transduction and inhibit cell proliferation and production of inflammatory mediators by synovial cells.
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Report
(4 results)
Research Products
(4 results)
