title: Impaired calcium signaling in muscle fibers from intercostal and foot skeletal muscle in a cigarette smoke-induced mouse model of COPD.
abstract: 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.
  
  
  
  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.
  
  
  
  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.
  
  
  
  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.
authors.affiliation: Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, 108 N. Greene Street, Baltimore, Maryland, 21201, USA.|Department of Physiology, Pennsylvania Muscle Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
authors.forename: Patrick
authors.initials: P
authors.lastname: Robison
authors.affiliation: Department of Environmental Health Sciences, Johns Hopkins University School of Public Health, Baltimore, Maryland, USA.
authors.forename: Thomas E
authors.initials: TE
authors.lastname: Sussan
authors.affiliation: Division of Biostatistics and Bioinformatics, Department of Epidemiology and Public Health, University of Maryland School of Medicine, Baltimore, Maryland, USA.
authors.forename: Hegang
authors.initials: H
authors.lastname: Chen
authors.affiliation: Department of Environmental Health Sciences, Johns Hopkins University School of Public Health, Baltimore, Maryland, USA.
authors.forename: Shyam
authors.initials: S
authors.lastname: Biswal
authors.affiliation: Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, 108 N. Greene Street, Baltimore, Maryland, 21201, USA.
authors.forename: Martin F
authors.initials: MF
authors.lastname: Schneider
authors.affiliation: Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, 108 N. Greene Street, Baltimore, Maryland, 21201, USA.
authors.forename: Erick O
authors.initials: EO
authors.lastname: Hernández-Ochoa
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000393:Air Pollutants / Q000633:toxicity; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000502:physiology*; D002147:Calmodulin / Q000378:metabolism; D004195:Disease Models, Animal; D005528:Foot / Q000294:innervation*; D005786:Gene Expression Regulation / Q000187:drug effects; D008124:Locomotion / Q000502:physiology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009119:Muscle Contraction; D018485:Muscle Fibers, Skeletal / Q000187:drug effects / Q000502:physiology*; D029424:Pulmonary Disease, Chronic Obstructive / Q000209:etiology* / Q000503:physiopathology*; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism; D009418:S100 Proteins / Q000378:metabolism; D012907:Smoking / Q000009:adverse effects*
chemical_list: D000393:Air Pollutants; D002147:Calmodulin; D019837:Ryanodine Receptor Calcium Release Channel; D009418:S100 Proteins; C110294:S100A1 protein; D002118:Calcium
keywords: COPD; Ca2+ transients; cigarette smoke; excitation-contraction coupling; locomotor muscle; respiratory muscle