Polyphenols prevent clinorotation-induced expression of atrogenes in mouse C2C12 skeletal myotubes

Area of Science:

• Cell Biology
• Molecular Biology
• Nutritional Science

Background:

• Oxidative stress stimulates atrogene expression, leading to skeletal muscle atrophy during unloading.
• Atrogenes are muscle atrophy-related ubiquitin ligases, crucial in muscle protein degradation.
• The impact of antioxidative nutrients on atrogene expression remains largely uninvestigated.

Purpose of the Study:

• To investigate the inhibitory effects of specific polyphenols on atrogene expression.
• To determine if these compounds can counteract atrogene upregulation induced by simulated unloading and glucocorticoids.
• To explore the role of ERK signaling in mediating these effects.

Main Methods:

• Utilized mouse C2C12 myoblasts and myotubes as a model system.
• Applied 3D-clinorotation and dexamethasone to induce atrogene expression.
• Assessed the expression of atrogenes (atrogin-1, MuRF-1) and ERK phosphorylation.
• Administered polyphenols including epicatechin (EC), epicatechin gallate (ECg), epigallocatechin gallate (EGCg), and quercetin.

Main Results:

• 3D-clinorotation and dexamethasone significantly increased atrogin-1 and MuRF-1 expression.
• EC, ECg, EGCg, and quercetin suppressed 3D-clinorotation-induced atrogene expression.
• These polyphenols showed minimal effect on dexamethasone-induced atrogene expression.
• Polyphenols significantly suppressed ERK phosphorylation, correlating with reduced atrogene expression.

Conclusions:

• Antioxidative nutrients, specifically catechins and quercetin, can suppress atrogene expression in skeletal muscle cells.
• The mechanism likely involves the inhibition of the ERK signaling pathway.
• These findings suggest a potential role for catechins and quercetin in preventing unloading-mediated muscle atrophy.