| Project/Area Number |
22790688
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Chiba University |
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Principal Investigator |
TAKANO Haruko 千葉大学, バイオメディカル研究センター, 機関研究員 (40532891)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 分子心臓病態学 / Ras-ERKカスケード / Rafファミリー / 肺胞形成 / II型肺胞上皮細胞 / 筋線維芽細胞 / 上皮間充織転換 / ノックアウトマウス / 発生・分化 / シグナル伝達 / 循環器・高血圧 / 細胞・組織 / 心肥大 |
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| Research Abstract |
We have identified DA-Raf (deleted A-Raf), which is generated by alternative splicing from Araf gene. It contains the Ras-binding domain, but lacks the kinase domain. To elucidate physiological functions of DA-Raf and their mechanisms, we generated DAraf gene-deficient (KO) mice, in which Araf expression is not affected. Lung alveoli were poorly developed due to the lack of myofibroblasts in the KO mice. On the other hand, alveolar epithelial type 2 cells (AEC2), which expressed DA-Raf at high level, might transform by epithelial-mesenchymal transition to myofibroblasts. These results imply that DA-Raf plays essential roles in alveolarization by regulating the Ras-ERK pathway in AEC2-myofibrblast transition.
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