| Project/Area Number |
22590801
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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 |
Circulatory organs internal medicine
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| Research Institution | Akita University |
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Principal Investigator |
ITO Hiroshi 秋田大学, 大学院・医学系研究科, 教授 (10232464)
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| Co-Investigator(Kenkyū-buntansha) |
WATANABE Hiroyuki 秋田大学, 医学系研究科, 医学系研究科 (80323145)
OHBA Takayoshi 秋田大学, 医学系研究科, 助教 (80431625)
NOBORO Kiyoshi 秋田大学, 医学部, 特任講師 (40436192)
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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 |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 心筋細胞肥大 / 細胞死 / Ca流入性TRPチャネル / STIM-1 / Ｃａ流入性ＴＲＰチャネル / ＳＴＩＭ１ / STIM1 |
|---|
| Research Abstract |
In cardiac hypertrophy model, we could detect increases in the expression of TRPC1,-C3, -C6, brain natriuretic peptide (BNP), and NFAT activity, Ca entry, as well as increases in cell surface area. Gene silencing of the TRPC1 and pharmacological treatment with a pyrazole derivative or sildenafil attenuate the Ca entry and prevent cardiac hypertrophy. In analysis of stromal interaction molecule 1 (STIM1; known as a Ca sensor of intracellular Ca store) knockout mice, we provide evidence that STIM1 together with TRPC1 is crucial for the development of cardiac hypertrophy. Moreover, STIM1 contributes to cardiac fibrosis under the condition of pressure over load. Ultimately, TRPC/STIM1 system might become novel pharmacological target in the treatment of cardiac hypertrophy.
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