Show simple item record Yu, Zengli en_US Li, Ping en_US Stamler, Jonathan en_US Yan, Zhen en_US 2011-06-21T17:31:23Z 2011-06-21T17:31:23Z 2008 en_US
dc.identifier.citation Yu,Zengli;Li,Ping;Zhang,Mei;Hannink,Mark;Stamler,Jonathan S.;Yan,Zhen. 2008. Fiber Type-Specific Nitric Oxide Protects Oxidative Myofibers against Cachectic Stimuli. Plos One 3(5): e2086-e2086. en_US
dc.identifier.issn 1932-6203 en_US
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. en_US
dc.language.iso en_US en_US
dc.relation.isversionof doi:10.1371/journal.pone.0002086 en_US
dc.subject biology en_US
dc.subject multidisciplinary sciences en_US
dc.title Fiber Type-Specific Nitric Oxide Protects Oxidative Myofibers against Cachectic Stimuli en_US
dc.title.alternative en_US
dc.description.version Version of Record en_US 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

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