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Impaired calcium signaling in muscle fibers from intercostal and foot skeletal muscle in a cigarette smoke‐induced mouse model of COPD
Author(s) -
Robison Patrick,
Sussan Thomas E.,
Chen Hegang,
Biswal Shyam,
Schneider Martin F.,
HernándezOchoa Erick O.
Publication year - 2017
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.25466
Subject(s) - copd , skeletal muscle , respiratory system , intercostal muscle , medicine , muscle contraction , pathophysiology , anatomy , endocrinology , contraction (grammar) , pathology
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 Ca 2+ signaling in excitation–contraction (E‐C) coupling is important for muscle activity, we hypothesized that Ca 2+ 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 Ca 2+ imaging and Western blot assays to assess Ca 2+ signals and E‐C coupling proteins. Results We found impaired Ca 2+ signals in muscle fibers from both muscle types, without significant changes in releasable Ca 2+ or in the expression levels of E‐C coupling proteins. Conclusions Ca 2+ 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