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

• Published in: Canadian journal of physiology and pharmacology 2011-01, Vol.89 (1), p.72-76
• Main Authors: Pellegrin, Maxime, Miguet-Alfonsi, Carole, Berthelot, Alain, Mazzolai, Lucia, Laurant, Pascal
• Format: Article
• Language: English
• Subjects: Akt-mediated eNOS phosphorylation; Animals; Biological and medical sciences; Care and treatment; Coronary heart disease; Endothelium; Enzymes; exercice de longue durée; Exercise; Fundamental and applied biological sciences. Psychology; Health aspects; healthy mice; long-term exercise; Male; Mice; Mice, Inbred C57BL; Nitric oxide; Nitric Oxide Synthase Type III - metabolism; Phosphorylation; Phosphorylation - physiology; phosphorylation de l'eNOS véhiculée par l'Akt; Physical Conditioning, Animal - physiology; Physiological aspects; Properties; Protein kinases; Proto-Oncogene Proteins c-akt - physiology; Random Allocation; Rodents; souris saine; Studies; Swimming; Swimming - physiology; Time Factors; Vertebrates: anatomy and physiology, studies on body, several organs or systems
• ISSN: 0008-4212; 1205-7541
• DOI: 10.1139/Y10-107

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.