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Regulation of eukaryotic initiation factor-2 expression during sepsis
T C Vary1, C V Jurasinski, A M Karinch
1Department of Cellular and Molecular Physiology, Pennsylvania State University, College of Medicine, Hershey 17033.
The American Journal of Physiology
|February 1, 1994
Summary
Sepsis differentially affects protein synthesis initiation. While liver protein synthesis increases due to more eukaryotic initiation factor-2 (eIF-2), skeletal muscle protein synthesis decreases because of reduced eIF-2B activity.
Area of Science:
- Biochemistry
- Molecular Biology
- Physiology
Background:
- Sepsis alters protein synthesis regulation.
- Differential effects on protein synthesis initiation are observed between liver and skeletal muscle during sepsis.
Purpose of the Study:
- Investigate mechanisms behind differential protein synthesis initiation changes in liver and skeletal muscle during sepsis.
- Measure cellular content of eukaryotic initiation factor-2 (eIF-2), eIF-2 alpha-subunit phosphorylation, and eIF-2B activity.
Main Methods:
- Assessed eIF-2 content, eIF-2 alpha phosphorylation, and eIF-2B activity in rat liver and skeletal muscle.
- Quantified eIF-2 alpha mRNA abundance and its association with polysomes.
Main Results:
- Skeletal muscle showed decreased eIF-2B activity but unchanged eIF-2 content and phosphorylation.
- Liver exhibited increased eIF-2 content, with no changes in eIF-2 alpha phosphorylation or eIF-2B activity.
- Both conditions saw increased polysomal association of eIF-2 alpha mRNA in liver.
Conclusions:
- Reduced eIF-2B activity is a key mechanism for inhibited protein synthesis in septic skeletal muscle.
- Increased eIF-2 levels and enhanced translation initiation contribute to stimulated protein synthesis in the liver during sepsis and sterile inflammation.