Project/Area Number |
26460268
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General anatomy (including histology/embryology)
|
Research Institution | Gunma University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
村上 徹 群馬大学, 大学院医学系研究科, 准教授 (10239494)
多鹿 友喜 群馬大学, 大学院医学系研究科, 講師 (90400738)
上野 仁之 群馬大学, 大学院医学系研究科, 助教 (30586251)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | シネミン / 中間径フィラメント / 骨格筋 / 肝臓 / 線維化 / 肝線維化 / 細胞骨格タンパク |
Outline of Final Research Achievements |
To reveal the functions of intermediate filament protein, synemin, we studied skeletal muscles and liver. In skeletal muscles, the interaction between actinin 3 (ACTN3) and synemin was studied using immunoprecipitation and fluorescence microscope. Co-precipitation and co-localization of these proteins were found. Whereas mice lacking ACTN3 showed improvement of endurance, those lacking synemin showed its decline. We are now studying the mechanisms of the latter. In the liver, synemin is expressed in stellate cells. In experimental fibrosis models of the liver, synemin knockout mice showed the reduction of fibrosis compared with that of the wild type animals. This might lead to the prevention and/or treatment of fibrosis in human liver.
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