| Project/Area Number |
22790929
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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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 | Kobe University |
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Principal Investigator |
SAEGUSA Jun 神戸大学, 医学部附属病院, 特定助教 (20514970)
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| Co-Investigator(Kenkyū-buntansha) |
MORINOBU Akio 神戸大学, 大学院・医学研究科, 准教授 (10294216)
KAWANO Seiji 神戸大学, 医学部附属病院, 特命准教授 (20351512)
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| Project Period (FY) |
2010 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2010: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | インテグリン / 増殖因子 / 関節リウマチ / 細胞増殖因子 / 滑膜細胞 |
|---|
| Research Abstract |
FGF and IGF are of interest in the initiation and development of RA synovial hyperplasia. We recently demonstrated that FGF1 binds directly to integrin αvβ3, and that an integrin-binding-defective FGF1 mutant (FGF^R50E) cannot induce cell proliferation; this is also true for IGF1. Here we investigated how the growth factor-integrin interaction is involved in growth factor signaling. The cDNA microarray analysis showed markedly reduced EGR-1 mRNA expression in the FGF^R50E-treated RA synoviocytes, compared to wild-type FGF1-treated cells. EGR-1 mRNA and protein were rapidly induced in RA synoviocytes in response to FGF1 or IGF1, but the EGR-1 expression was significantly impaired in FGF^R50E-or IGFR^36E/R37E-treated synoviocytes. The down-regulation of EGR-1 by siRNA facilitated the apoptosis of synoviocytes treated with H2O2 or etoposide.
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