Long-term exercise stabilizes atherosclerotic plaque in apolipoprotein-E deficient mice

Details

Serval ID
serval:BIB_97658A3B098A
Type
Article: article from journal or magazin.
Collection
Publications
Title
Long-term exercise stabilizes atherosclerotic plaque in apolipoprotein-E deficient mice
Journal
Medicine and Science in Sports and Exercise
Author(s)
Pellegrin M., Miguet-Alfonsi C., Bouzourene K., Aubert J.F., Deckert V., Berthelot A., Mazzolai L., Mach F., Haefliger J.A., Alonso F., Hayoz D.
ISSN
0195-9131
Publication state
Published
Issued date
2009
Peer-reviewed
Oui
Volume
41
Number
12
Pages
2128-2135
Language
english
Abstract
PURPOSE: Exercise is known to reduce cardiovascular mortality. However, the precise mechanisms are still unknown. Because atherosclerotic plaque destabilization and rupture leads to dramatic cardiovascular events, stabilization of plaque might be regarded as an important goal of an exercise preventive therapy. The present study examined the plaque-stabilizing effect of long-term exercise in experimental atherosclerosis using apolipoprotein E-deficient mice (ApoE(-/-)). METHODS: ApoE(-/-) mice were subjected to 6 months of swimming exercise. A group of sedentary animals were used as controls. Morphometry and characteristics of atherosclerotic plaque stability were assessed in aortic sinus by immunohistochemistry. Aortic levels of total protein kinase Akt (protein kinase B), phosphorylated Akt at Ser(473) (p-Akt), total endothelial nitric oxide synthase (eNOS), and phosphorylated eNOS at Ser(1177) (p-eNOS) were assessed by Western blotting. RESULTS: Exercised mice developed a more stable plaque phenotype as shown by decreased macrophage and increased smooth muscle cell content. Protein expressions of Akt, p-Akt, eNOS, and p-eNOS were not modulated by exercise. CONCLUSIONS: Long-term exercise promotes plaque stability in ApoE(-/-) mice. The Akt-mediated eNOS phosphorylation pathway seems not to be the primary molecular mechanism.
Keywords
Atherosclerosis, Swimming Exercise, Plaque Stability, Akt-Mediated Enos Phosphorylation, Coronary-Artery-Disease, E-Deficient Mice, Nitric-Oxide Synthase, Physical-Activity, Oxidative Stress, Endothelial Dysfunction, Inflammatory Markers, Aortic Endothelium, Rats, Risk
Pubmed
Web of science
Create date
13/10/2009 13:33
Last modification date
20/08/2019 14:59
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