Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pone.0002086
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dc.titleFiber type-specific nitric oxide protects oxidative myofibers against cachectic stimuli
dc.contributor.authorYu, Z.
dc.contributor.authorLi, P.
dc.contributor.authorZhang, M.
dc.contributor.authorHannink, M.
dc.contributor.authorStamler, J.S.
dc.contributor.authorYan, Z.
dc.date.accessioned2016-12-13T05:33:00Z
dc.date.available2016-12-13T05:33:00Z
dc.date.issued2008-05-07
dc.identifier.citationYu, Z., Li, P., Zhang, M., Hannink, M., Stamler, J.S., Yan, Z. (2008-05-07). Fiber type-specific nitric oxide protects oxidative myofibers against cachectic stimuli. PLoS ONE 3 (5) : -. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0002086
dc.identifier.issn19326203
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/132486
dc.description.abstractOxidative 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. © 2008 Yu et al.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1371/journal.pone.0002086
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentDUKE-NUS GRADUATE MEDICAL SCHOOL S'PORE
dc.description.doi10.1371/journal.pone.0002086
dc.description.sourcetitlePLoS ONE
dc.description.volume3
dc.description.issue5
dc.description.page-
dc.identifier.isiut000261642400009
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