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Effect of sepsis on eIE4E availability in skeletal muscle
1Department of Cellular and Molecular Physiology, The Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA.tvary@psu.edu
American Journal of Physiology. Endocrinology and Metabolism
|October 29, 2000
Summary
Sepsis inhibits protein synthesis in gastrocnemius muscle by impairing translation initiation. However, the eukaryotic initiation factor 4E (eIF4E) system is not the primary cause of this inhibition during sepsis.
Area of Science:
- Biochemistry
- Molecular Biology
- Physiology
Background:
- Sepsis leads to decreased protein synthesis in skeletal muscle, specifically the gastrocnemius.
- This inhibition is linked to impaired translation initiation, a critical step in protein synthesis.
Purpose of the Study:
- To investigate the impact of sepsis on the phosphorylation and availability of eukaryotic initiation factor 4E (eIF4E) in gastrocnemius muscle.
- To compare the effects of septic versus sterile abscesses on the eIF4E pathway.
Main Methods:
- Rats were subjected to sterile or septic abscess induction.
- Gastrocnemius muscle was analyzed 5 days post-induction for eIF4E phosphorylation, 4E-BP1 association and phosphorylation, and eIF4G binding to eIF4E.
- Cellular abundance of eIF4E was also assessed.
Main Results:
- Neither sepsis nor sterile inflammation affected eIF4E phosphorylation or 4E-BP1 binding/phosphorylation.
- Both sepsis and sterile inflammation reduced the binding of eIF4G to eIF4E.
- Sepsis, but not sterile inflammation, increased the cellular abundance of eIF4E.
Conclusions:
- Alterations in the eIF4E system do not appear to be the rate-limiting factor for protein synthesis in gastrocnemius muscle during sepsis.
- Previous findings suggest that changes in eIF2B are more likely responsible for limiting protein synthesis in skeletal muscle during sepsis.