Long-term swimming exercise does not modulate the Akt-dependent endothelial nitric oxide synthase phosphorylation in healthy mice.

Details

Serval ID
serval:BIB_758A7F58ACA0
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Long-term swimming exercise does not modulate the Akt-dependent endothelial nitric oxide synthase phosphorylation in healthy mice.
Journal
Canadian Journal of Physiology and Pharmacology
Author(s)
Pellegrin M., Miguet-Alfonsi C., Berthelot A., Mazzolai L., Laurant P.
ISSN
1205-7541 (Electronic)
ISSN-L
0008-4212
Publication state
Published
Issued date
2011
Volume
89
Number
1
Pages
72-76
Language
english
Notes
Publication types: Journal Article
Abstract
Molecular mechanisms by which exercise exerts cardiovascular benefits are poorly understood. Exercise-induced increase of endothelial NO synthase (eNOS) phosphorylation through the protein kinase Akt has been shown to be a key mechanism underlying the beneficial effect of exercise in coronary artery disease patients. We examined whether this protective pathway might also be activated in long-term-exercised healthy mice. C57BL/6 wild-type mice swam for 24 weeks. A group of sedentary animals were used as controls. Aortic levels of total protein kinase Akt (protein kinase B), phosphorylated Akt at ser473 (p-Akt), total eNOS, phosphorylated eNOS at Ser1177 (p-eNOS), and PECAM-1 (platelet endothelial cell adhesion molecule-1) were assessed by Western blotting. Protein expressions of Akt, p-Akt, eNOS, p-eNOS, and PECAM-1 were not modulated by 24 weeks of exercise. The Akt-dependent eNOS phosphorylation did not seem to be a primary molecular adaptation in response to long-term exercise in healthy mice.
Pubmed
Web of science
Create date
15/02/2011 12:03
Last modification date
20/08/2019 14:32
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