2011 Fiscal Year Final Research Report
Crosstalk between stress and cytokine signaling in metabolic syndrome
| 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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| 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 |
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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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[Journal Article] Reduction of TGF-β type II receptor is caused by the enhanced ubiquitin-dependent degradation in human renal cell carcinoma2010
Author(s)
H. Fukasawa, T. Yamamoto, Y. Fujigaki, T. Misaki, N. Ohashi, T. Takayama, S. Mugiya, T. Oda, C. Uchida, K. Kitagawa, T. Hattori, S. Suzuki, H. Hayashi, S. Ozono, M. Kitagawa, A. Hishida
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Journal Title
Int. J. Cancer
Volume: 127
Pages: 1517-1525
Peer Reviewed
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