Impaired calcium signaling in muscle fibers from intercostal and foot skeletal muscle in a cigarette smoke-induced mouse model of COPD

Patrick Robison, Thomas E. Sussan, Hegang Chen, Shyam Biswal, Martin F. Schneider, Erick O. Hernández-Ochoa

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish (US)
Pages (from-to)282-291
Number of pages10
JournalMuscle and Nerve
Volume56
Issue number2
DOIs
StatePublished - Aug 2017

Keywords

  • COPD
  • Ca transients
  • cigarette smoke
  • excitation-contraction coupling
  • locomotor muscle
  • respiratory muscle

ASJC Scopus subject areas

  • Physiology
  • Clinical Neurology
  • Cellular and Molecular Neuroscience
  • Physiology (medical)

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