Impairing eukaryotic elongation factor 2 kinase activity decreases atherosclerotic plaque formation.

Abstract

We tested whether loss of eukaryotic elongation factor 2 kinase (eEF2K) activity in macrophages suppresses development of atherosclerosis by transplanting bone marrow from mice with mutant eEF2K into ldlr(-/-) mice. Sixteen weeks after high-fat diet feeding, mutant eEF2K hematopoietic chimeras had a dramatically reduced level of atherosclerotic plaque formation. M1-skewed macrophages from eEF2K knock-in mice have less tumour necrosis factor-α release and a lesser ability to induce expression of endothelial cell markers, providing a potential explanation for the role of eEF2K. Because eEF2K activity in cells of the hematopoietic compartment contributes to atherosclerosis development, drugs inhibiting eEF2K might have a beneficial effect in treatment of atherosclerosis.

• Authors: Peng Zhang, Maziar Riazy, Matthew Gold, Shu-Huei Tsai, Kelly McNagny, Christopher Proud, Vincent Duronio
• Journal: The Canadian journal of cardiology (Can J Cardiol) Vol. 30 Issue 12 Pg. 1684-8 (Dec 2014) ISSN: 1916-7075 [Electronic] England
• PMID: 25475470 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2014 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.

Chemical References

• DNA
• Eef2k protein, mouse
• Elongation Factor 2 Kinase

Topics

• Animals
• DNA (genetics)
• Disease Models, Animal
• Elongation Factor 2 Kinase (biosynthesis, genetics)
• Gene Expression Regulation
• Mice
• Mice, Inbred C57BL
• Plaque, Atherosclerotic (enzymology, genetics, pathology)