Apoptosis invastus lateralismuscle of patients with COPD

Abstract

Peripheral muscle dysfunction is one of the most prominent systemic effects described in COPD patients and has important prognosis implications. The pathogenic mechanisms leading to muscle dysfunction/wasting are multifactorial and not fully understood. Apoptosis has been proposed as a contributor factor on this effect. Apoptosis was determined using two methodologies: immunoblotting to assess the protein levels of cleaved caspase-3 and the terminal deoxynucleotidyl transferase- mediated dUTP nick-end labeling (TUNEL) in paraffin-embedded sections from vastus lateralis specimens in COPD patients with low fat free mass index (FFMI) (COPD L ) (FEV 1 30±3.6 %pred, FFMI 15±0.2 Kg. m-2 ), ten patients with COPD and normal FFMI (COPD N ) (FEV 1 44±5.8 %pred, FFMI 19±0.5 Kg. m-2 ) and eight age and gender matched healthy controls (C) (FEV 1 95±3.9 %pred, FFMI 20±0.8 Kg. m-2 ). COPD L showed significantly higher levels of the cleaved caspase 3 in comparison to the COPD N and C (p<0.05). Figure 1: Protein levels of cleaved caspase 3 in vastus lateralis muscle of COPD patients with low fat free mass (COPD L ), COPD patients with normal fat free mass (COPD N ) and healthy controls (C). Results of the TUNEL assay show that the percentage of apoptotic nuclei was higher in COPD patients with low (55.7±25.48) and normal fat free mass (51.6±25.49) in comparison to C (37.5±37.51) (p=0.42). We conclude that apoptosis contributes to peripheral muscle wasting in this population of COPD patients.