Cigarette smoking induced decrease in fibronectin and COL1A1 in locomotor muscle in a guinea pig COPD model

Background: Sarcopenia is a major comorbidity in patients with chronic obstructive pulmonary disease (COPD) caused by decreased physical activity capacity, cigarette smoke (CS) and chronic hypoxia (CH). These risk factors affect muscle anabolic and catabolic biomarkers responsible for sarcopenia. However, whether CS and CH affect muscle extracellular matrix (ECM) biomarkers is still unknown. Intramuscular ECM plays an important role in muscle growth and repair processes, but their role in sarcopenia is under investigated. The aim of this study was to investigate alterations in the expression of intramuscular ECMs biomarkers in response to CH and CS. We hypothesize that altered expression of the ECM molecules promoted by CH and CS contribute to development of sarcopenia.
Methods: Skeletal muscle from a guinea pig animal model exposed (a) to 12 weeks CS (CS group), (b) to 10-week normal atmospheric air followed by 2-week of inspiratory oxygen fraction (FI,O2) of 0.12 in a hypoxic chamber (CH group), (c) to 12-week CS followed by 2-week CH (CS-CH group), (d) to 12-week sham CS followed by 2-week normal atmospheric air (Control group) were analysed by Real-time PCR for the change in expression of intramuscular ECM biomarkers.
Results: Only CS treatment induced significant decreased in fibronectin and COLA1 transcriptomes by 43% (p=0.05) and by 84.1% (p=0.026) respectively, compared to controls. CH and CS-CH treatment downregulated fibronectin and COLA1, but not significantly compared to controls. No significant differences in ECM gene expression were observed when comparing CH with CS treatment.
Conclusion: CS affects ECM composition altering the expression of fibronectin and COL1A1. The role of ECM biomarkers to muscle sarcopenia is being investigated.