NDLI: TNF signals via neuronal-type nitric oxide synthase and reactive oxygen species to depress specific force of skeletal muscle.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Stasko, Shawn A. Hardin, Brian J. Smith, Jeffrey D. Moylan, Jennifer S. Reid, Michael B.
Description	Country affiliation: United States Author Affiliation: Stasko SA ( Department of Physiology and Center for Muscle Biology, University of Kentucky, Lexington, Kentucky 40356-0298, USA.)
Abstract	TNF promotes skeletal muscle weakness, in part, by depressing specific force of muscle fibers. This is a rapid, receptor-mediated response, in which TNF stimulates cellular oxidant production, causing myofilament dysfunction. The oxidants appear to include nitric oxide (NO); otherwise, the redox mechanisms that underlie this response remain undefined. The current study tested the hypotheses that 1) TNF signals via neuronal-type NO synthase (nNOS) to depress specific force, and 2) muscle-derived reactive oxygen species (ROS) are essential co-mediators of this response. Mouse diaphragm fiber bundles were studied using live cell assays. TNF exposure increased general oxidant activity (P < 0.05; 2',7'-dichlorodihydrofluorescein diacetate assay) and NO activity (P < 0.05; 4-amino-5-methylamino-2',7'-difluorofluorescein diacetate assay) and depressed specific force across the full range of stimulus frequencies (1-300 Hz; P < 0.05). These responses were abolished by pretreatment with N(ω)-nitro-L-arginine methyl ester (L-NAME; a nonspecific inhibitor of NOS activity), confirming NO involvement. Genetic nNOS deficiency replicated L-NAME effects on TNF-treated muscle, diminishing NO activity (-80%; P < 0.05) and preventing the decrement in specific force (P < 0.05). Comparable protection was achieved by selective depletion of muscle-derived ROS. Pretreatment with either SOD (degrades superoxide anion) or catalase (degrades hydrogen peroxide) depressed oxidant activity in TNF-treated muscle and abolished the decrement in specific force. These findings indicate that TNF signals via nNOS to depress contractile function, a response that requires ROS and NO as obligate co-mediators.
File Format	HTM / HTML
ISSN	87507587
e-ISSN	15221601
DOI	10.1152/japplphysiol.00871.2012
Journal	Journal of Applied Physiology
Issue Number	11
Volume Number	114
Language	English
Publisher	American Physiological Society
Publisher Date	2013-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Physiology Diaphragm Physiology Muscle Strength Nitric Oxide Synthase Type I Metabolism Nitric Oxide Reactive Oxygen Species Tumor Necrosis Factor-alpha Animals Cells, Cultured Cytology Mice Mice, Inbred C57bl Mice, Knockout Signal Transduction Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Sports Science

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