Impaired myofibrillar function in the soleus muscle of mice with collagen-induced arthritis.

Détails

ID Serval
serval:BIB_8B7D9DF96539
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Impaired myofibrillar function in the soleus muscle of mice with collagen-induced arthritis.
Périodique
Arthritis and Rheumatism
Auteur(s)
Yamada T., Place N., Kosterina N., Ostberg T., Zhang S.J., Grundtman C., Erlandsson-Harris H., Lundberg I.E., Glenmark B., Bruton J.D., Westerblad H.
ISSN
0004-3591 (Print)
ISSN-L
0004-3591
Statut éditorial
Publié
Date de publication
2009
Volume
60
Numéro
11
Pages
3280-3289
Langue
anglais
Résumé
OBJECTIVE: Progressive muscle weakness is a common feature in patients with rheumatoid arthritis (RA). However, little is known about whether the intrinsic contractile properties of muscle fibers are affected in RA. This study was undertaken to investigate muscle contractility and the myoplasmic free Ca2+ concentration ([Ca2+](i)) in the soleus, a major postural muscle, in mice with collagen-induced arthritis (CIA).
METHODS: Muscle contractility and [Ca2+](i) were assessed in whole muscle and intact single-fiber preparations, respectively. The underlying mechanisms of contractile dysfunction were assessed by investigating redox modifications using Western blotting and antibodies against nitric oxide synthase (NOS), superoxide dismutase (SOD), 3-nitrotyrosine (3-NT), carbonyl, malondialdehyde (MDA), and S-nitrosocysteine (SNO-Cys).
RESULTS: The tetanic force per cross-sectional area was markedly decreased in the soleus muscle of mice with CIA, and the change was not due to a decrease in the amplitude of [Ca2+](i) transients. The reduction in force production was accompanied by slowing of the twitch contraction and relaxation and a decrease in the maximum shortening velocity. Immunoblot analyses showed a marked increase in neuronal NOS expression but not in inducible or endothelial NOS expression, which, together with the observed decrease in SOD2 expression, favors peroxynitrite formation. These changes were accompanied by increased 3-NT, carbonyl, and MDA adducts content in myofibrillar proteins from the muscles of mice with CIA. Moreover, there was a significant increase in SNO-Cys content in myosin heavy-chain and troponin I myofibrillar proteins from the soleus muscle of mice with CIA.
CONCLUSION: These findings show impaired contractile function in the soleus muscle of mice with CIA and suggest that this abnormality is due to peroxynitrite-induced modifications in myofibrillar proteins.
Mots-clé
Actins/metabolism, Animals, Arthritis, Experimental/metabolism, Arthritis, Experimental/physiopathology, Arthritis, Rheumatoid/metabolism, Arthritis, Rheumatoid/physiopathology, Body Weight/physiology, Disease Models, Animal, Female, Mice, Mice, Inbred DBA, Muscle Contraction/physiology, Muscle, Skeletal/physiopathology, Myofibrils/physiology, Myosin Heavy Chains/metabolism, Nitric Oxide Synthase/metabolism, Oxidation-Reduction, Peroxynitrous Acid/metabolism, Superoxide Dismutase/metabolism, Time Factors
Pubmed
Web of science
Création de la notice
20/09/2013 8:39
Dernière modification de la notice
20/08/2019 14:50
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