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Am J Physiol Heart Circ Physiol (December 5, 2002). doi:10.1152/ajpheart.00918.2002
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Articles in PresS, published online ahead of print December 5, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00918.2002
Submitted on October 24, 2002
Accepted on December 2, 2002

Role of c-Src in Regulation of Endothelial Nitric Oxide Synthase Expression During Exercise Training

Michael E Davis1, Hua Cai2, Louise McCann2, Tohru Fukai2, and David G Harrison1*

1 Division of Cardiology, Emory University, Atlanta, GA, USA; Department of Molecular and Systems Pharmacology Program, Emory University, Atlanta, GA, USA
2 Division of Cardiology, Emory University, Atlanta, GA, USA

* To whom correspondence should be addressed. E-mail: dharr02{at}emory.edu.

We have shown that c-Src plays a role in shear stress stimulation of endothelial nitric oxide synthase (eNOS) expression in cultured cells. To examine the role of c-Src in vivo, we exercised C57Blk/6 and c-Src heterozygous (c-Src+/-) mice on a treadmill for 3 weeks. Western analysis demonstrated that c-Src+/- mice express < 1/2 the normal amount of c-Src. Exercise increased heart rate and blood pressure to identical levels in both strains as determined using radiotelemetry. Exercise training increased eNOS protein > 2-fold in the aorta and 1.7-fold in the heart in C57Blk/6 while having no effect on eNOS protein levels in c-Src+/- mice. In contrast to exercise, treatment of mice with mevastatin, which stimulates expression of eNOS post-transcriptionally, increased eNOS expression in both strains. Training also increased aortic ecSOD protein expression, which is regulated by NO, only in C57Blk/6 mice while having no effect in c-Src+/- mice. These data indicate that c-Src has an important role in modulating vascular adaptations to exercise training, in particular increasing both eNOS and ecSOD protein expression.




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