BACKGROUND/AIMS: The molecular mechanisms leading to loss in muscle force during an acute exacerbation in COPD patients are unknown. A cross-sectional study was designed to compare the gene expression profile of the vastus lateralis muscle in patients with an acute COPD exacerbation and in stable COPD patients. METHODS: Muscle biopsies were taken in 9 COPD patients with an exacerbation on day 4 of hospitalization and in 15 stable COPD patients. Micro-array was performed on an UniSet Human 20K Bioarray. RESULTS: Gene Ontology and Gene Set Enrichment Analysis of the microarray data revealed enrichment of 1) the ubiquitin-dependent protein catabolism, the induction of apoptosis and anti-apoptosis and the response to reactive oxygen species in the upregulated transcripts, and 2) the aspartate catabolism and the mitochondrial respiratory chain in the downregulated transcripts. Real Time PCR data confirmed 1) increased expression of MuRF1 and MAFbx, markers of the ubiquitin dependent catabolism pathway, and 2) decreased expression levels of COX6C, a marker of mitochondrial respiration. CONCLUSIONS: The present study suggests that multiple pathways leading to muscle atrophy and mitochondrial dysfunction are altered in the muscle during an acute exacerbation. Strategies limiting the loss of muscle function during an acute exacerbation need to be developed. 2010 S. Karger AG, Basel.
BACKGROUND/AIMS: The molecular mechanisms leading to loss in muscle force during an acute exacerbation in COPDpatients are unknown. A cross-sectional study was designed to compare the gene expression profile of the vastus lateralis muscle in patients with an acute COPD exacerbation and in stable COPDpatients. METHODS: Muscle biopsies were taken in 9 COPDpatients with an exacerbation on day 4 of hospitalization and in 15 stable COPDpatients. Micro-array was performed on an UniSet Human 20K Bioarray. RESULTS: Gene Ontology and Gene Set Enrichment Analysis of the microarray data revealed enrichment of 1) the ubiquitin-dependent protein catabolism, the induction of apoptosis and anti-apoptosis and the response to reactive oxygen species in the upregulated transcripts, and 2) the aspartate catabolism and the mitochondrial respiratory chain in the downregulated transcripts. Real Time PCR data confirmed 1) increased expression of MuRF1 and MAFbx, markers of the ubiquitin dependent catabolism pathway, and 2) decreased expression levels of COX6C, a marker of mitochondrial respiration. CONCLUSIONS: The present study suggests that multiple pathways leading to muscle atrophy and mitochondrial dysfunction are altered in the muscle during an acute exacerbation. Strategies limiting the loss of muscle function during an acute exacerbation need to be developed. 2010 S. Karger AG, Basel.
Authors: Ramon C J Langen; Astrid Haegens; Juanita H J Vernooy; Emiel F M Wouters; Menno P J de Winther; Harald Carlsen; Chad Steele; Steven E Shoelson; Annemie M W J Schols Journal: Am J Respir Cell Mol Biol Date: 2012-04-26 Impact factor: 6.914
Authors: Esther Barreiro; Jacob I Sznajder; Gustavo A Nader; G R Scott Budinger Journal: Am J Respir Crit Care Med Date: 2015-03-15 Impact factor: 21.405
Authors: François Maltais; Marc Decramer; Richard Casaburi; Esther Barreiro; Yan Burelle; Richard Debigaré; P N Richard Dekhuijzen; Frits Franssen; Ghislaine Gayan-Ramirez; Joaquim Gea; Harry R Gosker; Rik Gosselink; Maurice Hayot; Sabah N A Hussain; Wim Janssens; Micheal I Polkey; Josep Roca; Didier Saey; Annemie M W J Schols; Martijn A Spruit; Michael Steiner; Tanja Taivassalo; Thierry Troosters; Ioannis Vogiatzis; Peter D Wagner Journal: Am J Respir Crit Care Med Date: 2014-05-01 Impact factor: 21.405