ArticleMolecular biology of the cell2019
Stretching magnitude-dependent inactivation of AKT by ROS led to enhanced p53 mitochondrial translocation and myoblast apoptosis.
Article in Molecular biology of the cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 17 citations in OpenAlex.
- Identifying regulators of aged fibroblast activation in 3D tissue models.Scientific reports · 2025Article
- Intensive stretch-activated CRT-PMCA1 feedback loop promoted apoptosis of myoblasts through CaApoptosis : an international journal on programmed cell death · 2022Article
- Autophagy in muscle regeneration: potential therapies for myopathies.Journal of cachexia, sarcopenia and muscle · 2022Review
- N-acetylcysteine promotes cyclic mechanical stress-induced osteogenic differentiation of periodontal ligament stem cells by down-regulating Nrf2 expression.Journal of dental sciences · 2022Article
- Effect of Quercetin on Dexamethasone-Induced C2C12 Skeletal Muscle Cell Injury.Molecules (Basel, Switzerland) · 2020Article
- P53 Regulates the Redox Status of Lung Endothelial Cells.Inflammation · 2020Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
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Abstract
Previously, we had shown that high magnitude stretch (HMS), rather than low magnitude stretch (LMS), induced significant apoptosis of skeletal muscle C2C12 myoblasts. However, the molecular mechanism remains obscure. In this study, we found that p53 protein accumulated in the nucleus of LMS-loaded cells, whereas it translocated into mitochondria of HMS-loaded cells. Knocking down endogenous p53 by shRNA abrogated HMS-induced apoptosis. Furthermore, we demonstrated that overaccumulation of reactive oxygen species (ROS) during HMS-inactivated AKT that was activated in LMS-treated cells, which accounted for the distinct p53 subcellular localizations under HMS and LMS. Blocking ROS generation by
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