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Acta Physiologica 2008; Volume 193, Supplement 664
Scandinavian Physiological Society’s Annual Meeting 2008
8/15/2008-8/17/2008
Oulu, Finland
CONTRACTILE DEFECTS AND PROTEIN NITRATION IN SLOW-TWITCH MUSCLE OF MICE WITH COLLAGEN-INDUCED ARTHRITIS
Abstract number: P39
YAMADA1 T, ZHANG1 SJ, BRUTON1 JD, WESTERBLAD1 H
1Dept of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
In patients with rheumatoid arthritis (RA), there is a progressive muscle weakness together with joint dysfunction. However, there is no data as to whether the muscle fibres' intrinsic contractile properties are affected in RA. We investigated the muscle contractility in slow- twitch soleus and fast-twitch extensor digitorum longus (EDL) muscle of mice with collagen- induced arthritis (CIA). The results show a markedly decreased force per cross-sectional area in soleus muscles but not in EDL muscles of CIA mice compared to control mice. To assess the underlying mechanism of this force deficit, we focused on the metabolism of reactive oxygen and nitrogen species. The results showed a marked increase in protein nitration in CIA soleus muscle and the extent of protein nitration correlated with the force decrease. In CIA soleus muscle there was a significant increase in neuronal nitric oxide synthase (NOS) expression but not in inducible or endothelial NOS expression. There was no difference in superoxide dismutase 1 or 2 expression between CIA and control soleus muscles. In conclusion, our results provide the first evidence that arthritis can cause decreased force production in slow-twitch muscle and that protein nitration appears to have a central role in this impairment.
To cite this abstract, please use the following information:
Acta Physiologica 2008; Volume 193, Supplement 664 :P39