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The effect of alpha7 acetylcholine receptor stimulation on muscle atrophy by inflammatory cytokines

Research Project

Project/Area Number 15K20027
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Anesthesiology
Research InstitutionAsahikawa Medical College

Principal Investigator

Sasakawa Tomoki  旭川医科大学, 医学部, 准教授 (30400112)

Research Collaborator Martyn Jeendra  ハーバード大学, 医学部, 教授
Project Period (FY) 2015-04-01 – 2018-03-31
Project Status Completed (Fiscal Year 2017)
Budget Amount *help
¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Keywordsアセチルコリン受容体 / 筋萎縮 / 炎症 / 敗血症 / 筋肥大 / ミトコンドリアバイオエナジェスティクス / α7AChR / ミトコンドリア
Outline of Final Research Achievements

Differentiation of myoblasts into myotubes in the presence of inflammatory cytokines was inhibited. In the absence of inflammatory cytokines, stimulation of α7 acetylcholine receptor by GTS21 increased myotube diameter and promoted expression of heavy chain myoglobin, but similar effects were not observed in the presence of inflammatory cytokines. In the presence of inflammatory cytokines it may be difficult to obtain a muscle hypertrophic effect by stimulation of GTS21. Previous published papers reported that muscle atrophy of mice was suppressed by administration of GTS 21 but the results of the present study are not due to direct action on muscle cells but the possibility that another mechanism of action may be involved.

Report

(4 results)
  • 2017 Annual Research Report   Final Research Report ( PDF )
  • 2016 Research-status Report
  • 2015 Research-status Report

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Published: 2015-04-16   Modified: 2019-03-29  

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