The molecular functions of Optineurin in the ALS pathogenesis

2016 Fiscal Year Final Research Report

• Project/Area Number: 25461280
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Neurology
• Research Institution: Hiroshima University
• Principal Investigator: NAGANO YOSHITO 広島大学, 医歯薬保健学研究院(医), 助教 (50397973)
• Co-Investigator(Renkei-kenkyūsha): KAWAKAMI Hideshi 広島大学, 原爆放射線医科学研究所, 教授 (70253060)
• Research Collaborator: YAO Tso-Pang Duke University, Professor
• Project Period (FY): 2013-04-01 – 2017-03-31
• Keywords: 筋萎縮性側索硬化症 / 筋萎縮 / Optineurin / C2C12

Outline of Final Research Achievements

To clarify the molecular functions of Optineurin(OPTN) which is one of ALS-causative gene, in muscle homeostasis, we used murine myoblast C2C12 cells. After differentiation to myotube, Tweak treatment could induce myotube atrophy. In this muscle atrophy model cells, OPTN expression levels of protein and mRNA were not changed during atrophy process. Furthermore OPTN knockdown by siRNA did not affect myotube atrophy induced by Tweak. On the other hand,OPTN may be involved in muscle differentiation process. OPTN protein expression was decreased gradually in that process,and OPTN knockdown promoted myogenic differentiation by regulating myogenic regulatory factor,such as Myf5. In summary, OPTN would not be involved in Tweak-induced muscle atrophy, however it may function as a negative regulator of muscle differentiation.

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