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The analysis of potassium channel as mechanosensors in osteocytes

Research Project

Project/Area Number 25293319
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypePartial Multi-year Fund
Section一般
Research Field Orthopaedic surgery
Research InstitutionGifu University

Principal Investigator

AKIYAMA HARUHIKO  岐阜大学, 医学(系)研究科(研究院), 教授 (60402830)

Co-Investigator(Kenkyū-buntansha) 松田 秀一  京都大学, 医学(系)研究科(研究院), 教授 (40294938)
宿南 知佐  広島大学, 医歯薬保健学研究院, 教授 (60303905)
Project Period (FY) 2013-04-01 – 2017-03-31
Project Status Completed (Fiscal Year 2016)
Budget Amount *help
¥17,940,000 (Direct Cost: ¥13,800,000、Indirect Cost: ¥4,140,000)
Fiscal Year 2016: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2015: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2014: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2013: ¥6,890,000 (Direct Cost: ¥5,300,000、Indirect Cost: ¥1,590,000)
Keywords廃用性骨萎縮 / カリウムチャネル / ノックアウトマウス / イオンチャネル / 骨萎縮 / 骨細胞
Outline of Final Research Achievements

To clarify molecular mechanisms under disuse bone atrophy, we generated the mice with ligation of ischia nerve, and analyzed gene expression profiles of the femurs, resulting in identification of Kcnmb1 and Kcnmb4. These genes are expressed in osteocytes and periosteal cells, and the expression of these genes were down regulated in disuse bone atrophy model mice. In double knockout mice of Kcnmb1 and Kcnmb4, the bone volume of these mice significantly increased. These data strongly suggest that Kcnmb1 and Kcnmb4 are involved in disuse bone atrophy.

Report

(5 results)
  • 2016 Annual Research Report   Final Research Report ( PDF )
  • 2015 Annual Research Report
  • 2014 Annual Research Report
  • 2013 Annual Research Report

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Published: 2013-05-21   Modified: 2019-07-29  

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