Abstract:
INTRODUCTION:Respiratory and locomotor skeletal muscle dysfunction are common findings in chronic obstructive pulmonary disease (COPD); however, the mechanisms that cause muscle impairment in COPD are unclear. Because Ca2+ signaling in excitation-contraction (E-C) coupling is important for muscle activity, we hypothesized that Ca2+ dysregulation could contribute to muscle dysfunction in COPD. METHODS:Intercostal and flexor digitorum brevis muscles from control and cigarette smoke-exposed mice were investigated. We used single cell Ca2+ imaging and Western blot assays to assess Ca2+ signals and E-C coupling proteins. RESULTS:We found impaired Ca2+ signals in muscle fibers from both muscle types, without significant changes in releasable Ca2+ or in the expression levels of E-C coupling proteins. CONCLUSIONS:Ca2+ dysregulation may contribute or accompany respiratory and locomotor muscle dysfunction in COPD. These findings are of significance to the understanding of the pathophysiological course of COPD in respiratory and locomotor muscles. Muscle Nerve 56: 282-291, 2017.
journal_name
Muscle Nervejournal_title
Muscle & nerveauthors
Robison P,Sussan TE,Chen H,Biswal S,Schneider MF,Hernández-Ochoa EOdoi
10.1002/mus.25466subject
Has Abstractpub_date
2017-08-01 00:00:00pages
282-291issue
2eissn
0148-639Xissn
1097-4598journal_volume
56pub_type
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