Alterations in Skeletal Muscle Cell Homeostasis in a Mouse Model of Cigarette Smoke Exposure

Skeletal muscle dysfunction is common in chronic obstructive pulmonary disease (COPD), a disease mainly caused by chronic cigarette use. An important proportion of patients with COPD have decreased muscle mass, suggesting that chronic cigarette smoke exposure may interfere with skeletal muscle cellu...

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Veröffentlicht in:	PloS one Jg. 8; H. 6; S. e66433
Hauptverfasser:	Caron, Marc-André, Morissette, Mathieu C., Thériault, Marie-Eve, Nikota, Jake K., Stämpfli, Martin R., Debigaré, Richard
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	United States Public Library of Science 14.06.2013 Public Library of Science (PLoS)
Schlagworte:	AKT protein Alterations Analysis Animals Biodegradation Biology Chronic obstructive pulmonary disease Cigarette smoke Cigarettes Degradation Dietary fiber Drug addiction Exposure Female Gene expression Glycogen Glycogen synthase kinase 3 Glycogen synthesis Growth factors Homeostasis Immunology Kinases Lung diseases Medicine Mice Mice, Inbred BALB C mRNA Muscle Fibers, Skeletal - drug effects Muscle Fibers, Skeletal - metabolism Muscle, Skeletal - drug effects Muscle, Skeletal - pathology Muscles Musculoskeletal system Nicotiana - adverse effects Obstructive lung disease Organ Size Pathology Phosphorylation Plant Extracts - pharmacology Protein biosynthesis Protein Biosynthesis - drug effects Protein synthesis Proteins Proteolysis - drug effects Pulmonary Disease, Chronic Obstructive - etiology Pulmonary Disease, Chronic Obstructive - pathology RNA Rodents Signal Transduction Signaling Skeletal muscle Smoke Smoke - adverse effects Smoking Smoking - adverse effects Smoking cessation Tumor necrosis factor-TNF Ventilation Ontario Canada Canada Quebec City Quebec Canada
ISSN:	1932-6203, 1932-6203
Online-Zugang:	Volltext
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Zusammenfassung:	Skeletal muscle dysfunction is common in chronic obstructive pulmonary disease (COPD), a disease mainly caused by chronic cigarette use. An important proportion of patients with COPD have decreased muscle mass, suggesting that chronic cigarette smoke exposure may interfere with skeletal muscle cellular equilibrium. Therefore, the main objective of this study was to investigate the kinetic of the effects that cigarette smoke exposure has on skeletal muscle cell signaling involved in protein homeostasis and to assess the reversibility of these effects. A mouse model of cigarette smoke exposure was used to assess skeletal muscle changes. BALB/c mice were exposed to cigarette smoke or room air for 8 weeks, 24 weeks or 24 weeks followed by 60 days of cessation. The gastrocnemius and soleus muscles were collected and the activation state of key mediators involved in protein synthesis and degradation was assessed. Gastrocnemius and soleus were smaller in mice exposed to cigarette smoke for 8 and 24 weeks compared to room air exposed animals. Pro-degradation proteins were induced at the mRNA level after 8 and 24 weeks. Twenty-four weeks of cigarette smoke exposure induced pro-degradation proteins and reduced Akt phosphorylation and glycogen synthase kinase-3β quantity. A 60-day smoking cessation period reversed the cell signaling alterations induced by cigarette smoke exposure. Repeated cigarette smoke exposure induces reversible muscle signaling alterations that are dependent on the duration of the cigarette smoke exposure. These results highlights a beneficial aspect associated with smoking cessation.
Bibliographie:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Conceived and designed the experiments: MAC MCM MRS RD. Performed the experiments: MAC MCM MET JKN. Analyzed the data: MAC MCM MRS RD. Contributed reagents/materials/analysis tools: MRS RD. Wrote the paper: MAC MCM MRS RD. Competing Interests: The authors have declared that no competing interests exist.
ISSN:	1932-6203 1932-6203
DOI:	10.1371/journal.pone.0066433