NDLI: L-arginine decreases inflammation and modulates the nuclear factor-kappaB/matrix metalloproteinase cascade in mdx muscle fibers.

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Year: 2008 Volume: 172 Issue: 5

Year: 2004 Volume: 164

L-arginine decreases inflammation and modulates the nuclear factor-kappaB/matrix metalloproteinase cascade in mdx muscle fibers.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Hnia, Karim Gayraud, Jérôme Hugon, Gérald Ramonatxo, Michèle De La Porte, Sabine Matecki, Stefan Mornet, Dominique
Description	Country affiliation: France Author Affiliation: Hnia K ( INSERM ERI 25 Muscle et Pathologies, CHU A. de Villeneuve, Université de Montpellier1, EA 4202, 34295 Montpellier Cedex 5, France.)
Abstract	Duchenne muscular dystrophy (DMD) is a lethal, X-linked disorder associated with dystrophin deficiency that results in chronic inflammation, sarcolemma damage, and severe skeletal muscle degeneration. Recently, the use of L-arginine, the substrate of nitric oxide synthase (nNOS), has been proposed as a pharmacological treatment to attenuate the dystrophic pattern of DMD. However, little is known about signaling events that occur in dystrophic muscle with l-arginine treatment. Considering the implication of inflammation in dystrophic processes, we asked whether L-arginine inhibits inflammatory signaling cascades. We demonstrate that L-arginine decreases inflammation and enhances muscle regeneration in the mdx mouse model. Classic stimulatory signals, such as proinflammatory cytokines interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha, are significantly decreased in mdx mouse muscle, resulting in lower nuclear factor (NF)-kappaB levels and activity. NF-kappaB serves as a pivotal transcription factor with multiple levels of regulation; previous studies have shown perturbation of NF-kappaB signaling in both mdx and DMD muscle. Moreover, L-arginine decreases the activity of metalloproteinase (MMP)-2 and MMP-9, which are transcriptionally activated by NF-kappaB. We show that the inhibitory effect of L-arginine on the NF-kappaB/MMP cascade reduces beta-dystroglycan cleavage and translocates utrophin and nNOS throughout the sarcolemma. Collectively, our results clarify the molecular events by which L-arginine promotes muscle membrane integrity in dystrophic muscle and suggest that NF-kappaB-related signaling cascades could be potential therapeutic targets for DMD management.
File Format	HTM / HTML
ISSN	00029440
e-ISSN	15252191
DOI	10.2353/ajpath.2008.071009
Journal	The American Journal of Pathology
Issue Number	6
Volume Number	172
Language	English
Publisher	Elsevier (on behalf of the American Society for Investigative Pathology)
Publisher Date	2008-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Nf-kappa B Research Support, Non-u.s. Gov't Signal Transduction Matrix Metalloproteinase 2 Drug Therapy Discipline Pathology Pharmacology Inflammation Metabolism Pathology Regeneration Animals Arginine Muscle Fibers, Skeletal Mice, Inbred Mdx Nitric Oxide Synthase Physiology Mice Muscle, Skeletal Muscular Dystrophy, Duchenne Map Kinase Signaling System Matrix Metalloproteinase 9
Content Type	Text
Resource Type	Article
Subject	Pathology and Forensic Medicine

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