| Project/Area Number |
21590067
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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 |
Biological pharmacy
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| Research Institution | Nagoya City University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
ITOH Yuka 名古屋市立大学, 大学院・薬学研究科, 助教 (40454326)
SAKAI Satoshi 新潟薬科大学, 薬学部, 助教 (50566081)
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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: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ストレス / TRB3 / TGFβ / 脂肪細胞 / β細胞 / メタボリックシンドローム / TRB1 / 小胞体ストレス / PPARγ / IL-2 / perilipin / 脂肪組胞 / 脂肪滴 / Smad3 / 肝細胞 / Cdc25A / 膵β細胞 / C / EBPβ / RORα |
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| Research Abstract |
In this study, we examined the crosstalk between stress and inflammatory cytokine signaling in metabolic syndrome using adipocytes, hepatocytes and pancreatic beta cells, especially focused on contribution of the members of pseudokinase family TRBs, which are induced by various stresses.
Both signals were strongly attenuated the maturation and function of adipocytes(3T3-L1 cells and HW11 cells). On the other hand, in human hepatoma cell line, HepG2 cells, stress induced TRB3 potently inhibited the signaling of one of the inflammatory cytokines, TGFβ. Moreover the impairment ofβcell line, Min6 cells, induced by endoplasmic reticulum stress is rescued by TGFβ. Our findings suggest that the crosstalk of both signal showed the cell-specific phenotype, and that TRBs proteins function as the tuner of these responses.
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