| Project/Area Number |
21591466
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Dermatology
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| Research Institution | 高知県立大学 (2011)
Kochi Women's University (2009-2010) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TERAISHI Mika 高知大学, 医学部付属病院, 医員 (40437736)
SANO Shigetoshi 高知大学, 教育研究部医療学系, 教授 (80273621)
SHIGA Takeo 高知大学, 医学部付属病院, 医員 (70444768)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 皮膚炎症 / 再生学 / 膠原病 / 強皮症 / 線維芽細胞 / コラーゲン / Smad / Smad interacting protein 1 / TGF-β / Smad interacting protein 1(SIP1/ZEB2) / Smad interacting protein 1 (SIP1 / ZEB2) |
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| Research Abstract |
We generated mesodermal-specific SIP1 knockout mice. The expression of type I and type III collagen mRNA in the fibroblasts of the mice was suppressed, while MMP13 mRNA expression was up-regulated. The mice showed thinning of dermis and subcutaneous fatty tissue. The injected sites of bleomycin, a skin fibrosis inducer, showed attenuated fibrosis in the mice. Although SIP1 suppressed the expression of E-cadherin in the process of epithelial-mesenchymal transition, SIP1 promoted the collagen production in the process of skin fibrosis. We consider that SIP1 is one of the target molecules for the treatment of scleroderma.
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