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dc.contributor.author Yu, Z
dc.contributor.author Li, P
dc.contributor.author Zhang, M
dc.contributor.author Hannink, M
dc.contributor.author Stamler, JS
dc.contributor.author Yan, Z
dc.coverage.spatial United States
dc.date.accessioned 2011-06-21T17:31:23Z
dc.date.issued 2008-05-07
dc.identifier http://www.ncbi.nlm.nih.gov/pubmed/18461174
dc.identifier.citation PLoS One, 2008, 3 (5), pp. e2086 - ?
dc.identifier.uri http://hdl.handle.net/10161/4488
dc.description.abstract Oxidative skeletal muscles are more resistant than glycolytic muscles to cachexia caused by chronic heart failure and other chronic diseases. The molecular mechanism for the protection associated with oxidative phenotype remains elusive. We hypothesized that differences in reactive oxygen species (ROS) and nitric oxide (NO) determine the fiber type susceptibility. Here, we show that intraperitoneal injection of endotoxin (lipopolysaccharide, LPS) in mice resulted in higher level of ROS and greater expression of muscle-specific E3 ubiqitin ligases, muscle atrophy F-box (MAFbx)/atrogin-1 and muscle RING finger-1 (MuRF1), in glycolytic white vastus lateralis muscle than in oxidative soleus muscle. By contrast, NO production, inducible NO synthase (iNos) and antioxidant gene expression were greatly enhanced in oxidative, but not in glycolytic muscles, suggesting that NO mediates protection against muscle wasting. NO donors enhanced iNos and antioxidant gene expression and blocked cytokine/endotoxin-induced MAFbx/atrogin-1 expression in cultured myoblasts and in skeletal muscle in vivo. Our studies reveal a novel protective mechanism in oxidative myofibers mediated by enhanced iNos and antioxidant gene expression and suggest a significant value of enhanced NO signaling as a new therapeutic strategy for cachexia.
dc.format.extent e2086 - ?
dc.language ENG
dc.language.iso en_US en_US
dc.relation.ispartof PLoS One
dc.relation.isversionof 10.1371/journal.pone.0002086
dc.subject Animals
dc.subject Antioxidants
dc.subject Atrophy
dc.subject Cachexia
dc.subject Endotoxins
dc.subject Gene Expression Regulation
dc.subject Glycolysis
dc.subject Mice
dc.subject Molecular Sequence Data
dc.subject Muscle Fibers, Skeletal
dc.subject Muscle, Skeletal
dc.subject Nitric Oxide
dc.subject Oxidative Stress
dc.subject Reactive Oxygen Species
dc.subject S-Nitrosoglutathione
dc.title Fiber type-specific nitric oxide protects oxidative myofibers against cachectic stimuli.
dc.title.alternative en_US
dc.type Journal Article
dc.description.version Version of Record en_US
duke.date.pubdate 2008-5-7 en_US
duke.description.endpage e2086 en_US
duke.description.issue 5 en_US
duke.description.startpage e2086 en_US
duke.description.volume 3 en_US
dc.relation.journal Plos One en_US
pubs.author-url http://www.ncbi.nlm.nih.gov/pubmed/18461174
pubs.issue 5
pubs.organisational-group /Duke
pubs.organisational-group /Duke/School of Medicine
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Medicine
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Medicine/Medicine, Pulmonary, Allergy, and Critical Care Medicine
pubs.publication-status Published online
pubs.volume 3
dc.identifier.eissn 1932-6203

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