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Publication : Chronic Exercise Training Improved Aortic Endothelial and Mitochondrial Function via an AMPKα2-Dependent Manner.

First Author  Chen X Year  2016
Journal  Front Physiol Volume  7
Pages  631 PubMed ID  28066264
Mgi Jnum  J:292904 Mgi Id  MGI:6437589
Doi  10.3389/fphys.2016.00631 Citation  Chen X, et al. (2016) Chronic Exercise Training Improved Aortic Endothelial and Mitochondrial Function via an AMPKalpha2-Dependent Manner. Front Physiol 7:631
abstractText  Chronic exercise training is known to protect the vasculature; however, the underlying mechanisms remain obscure. The present study hypothesized that exercise may improve aortic endothelial and mitochondrial function through an adenosine monophosphate-activated protein kinase alpha2 (AMPKalpha2)-dependent manner. Ten-week-old AMPKalpha2 knockout (AMPKalpha2(-/-)) mice and age-matched wild-type (WT) mice were subjected to daily treadmill running for 6 weeks, and the thoracic aorta from these mice were used for further examination. Our results showed that exercise significantly promoted vasodilatation and increased expression and phosphorylation of endothelial nitric oxide synthase (eNOS), concomitant with increased AMPKalpha2 expression in WT mice. These effects were not observed in AMPKalpha2(-/-) mice. Furthermore, exercise training increased thoracic aortic mitochondrial content as indicated by increased Complex I and mitochondrial DNA (mtDNA) in WT mice but not in AMPKalpha2(-/-) mice. This may be caused by decreased mitochondrial autophagy since the expression of BH3 domain-containing BCL2 family members BNIP3-like (BNIP3L) and LC3B were decreased in WT mice with exercise. And these changes were absent with AMPKalpha2 deletion in mice. Importantly, exercise increased the expression of manganous superoxide dismutase (MnSOD) and catalase, suggesting that mitochondrial antioxidative capacity was increased. Notably, the improved antioxidative capacity was lost in AMPKalpha2(-/-) mice with exercise. In conclusion, this study illustrated that AMPKalpha2 plays a critical role in exercise-related vascular protection via increasing endothelial and mitochondrial function in the artery.
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