| Project/Area Number |
22591138
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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 |
Pediatrics
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| Research Institution | Jikei University School of Medicine |
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Principal Investigator |
MIYATA Ichiro 東京慈恵会医科大学, 医学部, 准教授 (10200180)
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| Co-Investigator(Renkei-kenkyūsha) |
URASHIMA Takashi 東京慈恵会医科大学, 医学部, 講師 (20338875)
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| Research Collaborator |
MOTOKI Takanori 東京慈恵会医科大学, 医学部, 助教 (80596263)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2012: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
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 | 左心負荷モデルラット / Urocortin-2 / Urocortin-3 / TNFα / IL-6 / SOCS-3 / c-fos / Nesfatin-1 / Urocortin 2 / Urocortin 3 / 神経内分泌学 / CRF-R2α / 左心不全ラット / Urocortin 1 / Amygdala / Hypothalamus |
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| Research Abstract |
Our results indicate that Ucn-2 and Ucn-3 can be sensitive markers for left ventricular heart loading, and endogenous Ucn-2 and Ucn-3 through CRF-R2 are critical molecular mediators of the physiological response to heart failure in the central nervous system as well as in the heart. Taken together, our data suggest that left ventricular heart loading induces the increase of inflammatory cytokines such as IL-6, and affects the negative feedback system of cytokine signalings in the brain.Furthermore, it is speculated that Ucn-3 may play an important role in the energy homeostasis through the different pathway from Nesfatin-1 under condition of left ventricular heart failure.
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