Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 409, Issue 2, Pages 217-221Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2011.04.122
Keywords
Angiotensin II; Skeletal muscle; Oxidative stress; NADPH oxidase; Atrophy
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Funding
- National Institutes of Health/National Heart, Lung and Blood Institute [R01HL070241, R01HL080682]
- National Institutes of Health / National Center for Research Resources [P20RR018766]
- National Institute of Health/National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) [7K99DK083455-02]
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Angiotensin II (Ang II) causes skeletal muscle wasting via an increase in muscle catabolism. To determine whether the wasting effects of Ang II were related to its ability to increase NADPH oxidase-derived reactive oxygen species (ROS) we infused wild-type C57BL/6J or p47(Phox-/-) mice with vehicle or Ang II for 7 days. Superoxide production was increased 2.4-fold in the skeletal muscle of Ang II infused mice, and this increase was prevented in p47(Phox-/-) mice. Apocynin treatment prevented Ang II-induced superoxide production in skeletal muscle, consistent with Ang II increasing NADPH oxidase derived ROS. Ang II induced loss of body and skeletal muscle weight in C57BL/6J mice, whereas the reduction was significantly attenuated in p47(Phox-/-) animals. The reduction of skeletal muscle weight caused by Ang II was associated with an increase of proteasome activity, and this increase was completely prevented in the skeletal muscle of p47(Phox-/-) mice. In conclusion, Ang II-induced skeletal muscle wasting is in part dependent on NADPH oxidase derived ROS. (C) 2011 Elsevier Inc. All rights reserved.
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