Nitrosative modifications of the Ca2+ release complex and actin underlie arthritis-induced muscle weakness.

ABSTRACT:

Objective

Skeletal muscle weakness is a prominent clinical feature in patients with rheumatoid arthritis (RA), but the underlying mechanism(s) is unknown. Here we investigate the mechanisms behind arthritis-induced skeletal muscle weakness with special focus on the role of nitrosative stress on intracellular Ca(2+) handling and specific force production.

Methods

Nitric oxide synthase (NOS) expression, degree of nitrosative stress and composition of the major intracellular Ca(2+) release channel (ryanodine receptor 1, RyR1) complex were measured in muscle. Changes in cytosolic free Ca(2+) concentration ([Ca(2+)]i) and force production were assessed in single-muscle fibres and isolated myofibrils using atomic force cantilevers.

Results

The total neuronal NOS (nNOS) leve

SUBMITTER: Yamada T 

PROVIDER: S-EPMC4602262 | biostudies-literature | 2015 Oct

REPOSITORIES: biostudies-literature