宇宙医学から健康長寿へ : 第258回徳島医学会学術集会公開シンポジウム

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  • ウチュウ イガク カラ ケンコウ チョウジュ エ : ダイ258カイ トクシマ イガッカイ ガクジュツ シュウカイ コウカイ シンポジウム
  • The mechanism of skeletal muscle atrophy : finding from space experiment

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Skeletal muscle atrophy is a response to decreased physical signals (unloading), such as under microgravity, bed rest and neural inactivation, and is characterized by muscle volume loss and muscle fiber-type switching. We previously demonstrated that elevated ubiquitin ligase casitas B-lineage lymphoma-b (Cbl-b) resulted in the loss of muscle volume. Here, we showed that the ROS-mediated signal transduction caused by microgravity or its simulation contributes to Cbl-b expression. In L6 myotubes, the assessment of redox status revealed that oxidized glutathione was increased under microgravity conditions, and simulated microgravity caused a burst of ROS, implicating ROS as a critical upstream mediator linking to downstream atrophic signaling. ROS generation activated the ERK 1/2 early-growth response protein (Egr) 1/2-Cbl-b signaling pathway. Our results suggest that under microgravity conditions, elevated ROS may be a crucial mechanotransducer in skeletal muscle cells, regulating muscle mass through Cbl-b expression activated by the ERK-Egr signaling pathway.

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