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Cited by 88Muscle Physiology and DisordersChronic Obstructive Pulmonary Disease (COPD) ResearchNutrition and Health in Aging

Genome-Wide MRNA Expression Profiling in Vastus Lateralis of COPD Patients with Low and Normal Fat Free Mass Index and Healthy Controls

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Rabinovich, Roberto A, Drost, Ellen, Manning, Jonathan R, Dunbar, Donald R, Díaz-Ramos, MaCarmen, Lakhdar, Ramzi, Bastos, Ricardo, MacNee, William·2015·Respiratory Research
DOI 10.1186/s12931-014-0139-5PMC PMC4333166
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Abstract

BACKGROUND: Chronic Obstructive Pulmonary Disease (COPD) has significant systemic effects beyond the lungs amongst which muscle wasting is a prominent contributor to exercise limitation and an independent predictor of morbidity and mortality. The molecular mechanisms leading to skeletal muscle dysfunction/wasting are not fully understood and are likely to be multi-factorial. The need to develop therapeutic strategies aimed at improving skeletal muscle dysfunction/wasting requires a better understanding of the molecular mechanisms responsible for these abnormalities. Microarrays are powerful tools that allow the investigation of the expression of thousands of genes, virtually the whole genome, simultaneously. We aim at identifying genes and molecular pathways involved in skeletal muscle wasting in COPD. METHODS: We assessed and compared the vastus lateralis transcriptome of COPD patients with low fat free mass index (FFMI) as a surrogate of muscle mass (COPDL) (FEV1 30 ± 3.6%pred, FFMI 15 ± 0.2 Kg.m(-2)) with patients with COPD and normal FFMI (COPDN) (FEV1 44 ± 5.8%pred, FFMI 19 ± 0.5 Kg.m(-2)) and a group of age and sex matched healthy controls (C) (FEV1 95 ± 3.9%pred, FFMI 20 ± 0.8 Kg.m(-2)) using Agilent Human Whole Genome 4x44K microarrays. The altered expression of several of these genes was confirmed by real time TaqMan PCR. Protein levels of P21 were assessed by immunoblotting. RESULTS: A subset of 42 genes was differentially expressed in COPDL in comparison to both COPDN and C (PFP < 0.05; -1.5 ≥ FC ≥ 1.5). The altered expression of several of these genes was confirmed by real time TaqMan PCR and correlated with different functional and structural muscle parameters. Five of these genes (CDKN1A, GADD45A, PMP22, BEX2, CGREF1, CYR61), were associated with cell cycle arrest and growth regulation and had been previously identified in studies relating muscle wasting and ageing. Protein levels of CDKN1A, a recognized marker of premature ageing/cell cycle arrest, were also found to be increased in COPDL. CONCLUSIONS: This study provides evidence of differentially expressed genes in peripheral muscle in COPD patients corresponding to relevant biological processes associated with skeletal muscle wasting and provides potential targets for future therapeutic interventions to prevent loss of muscle function and mass in COPD.

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  • An increase in SLC22A3 had also been reported in COPD genome in GWAS.

    “Such increase had also been reported in COPD genome in genome-wide association studies (GWAS) [139].”

    From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [139]

    The Results (Global assessment of gene expression, Table 4; page unavailable) report increased SLC22A3 expression in vastus lateralis muscle from COPD patients with low fat-free mass. The Methods (Microarray hybridization and data analysis; page unavailable) describe RNA-expression profiling, not a genome-wide association study. Thus the increase is supported, but its attribution to GWAS or the COPD genome is not. (LLM, conf=0.88)

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Cited by

Sorted by citations

Authors
Rabinovich, R. A., Drost, E., Manning, J. R., Dunbar, D. R., Díaz-Ramos, M., Lakhdar, R., Bastos, R., & MacNee, W.
Affiliations
  • Centre for Inflammation Research (GB)
  • University of Edinburgh (GB)
  • Consorci Institut D'Investigacions Biomediques August Pi I Sunyer (ES)
  • Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (ES)
Corresponding author
Rabinovich, Roberto A
ORCID
Venue
Respiratory Research
Publisher
Springer Science and Business Media LLC
Published
2015-01-08
Volume
16
Issue
1
Pages
1-1
ISSN
  • 1465-9921 (ISSN-L)
  • 1465-993X
DOI
10.1186/s12931-014-0139-5
PMC
PMC4333166
OpenAlex
W2141536507
Cited by
88
References
9
Citations by year
2026: 1 · 2025: 3 · 2024: 4 · 2023: 6 · 2022: 2 · 2021: 18 · 2020: 10 · 2019: 10 · 2018: 15 · 2017: 12 · 2016: 4 · 2015: 3
FWCI
4.92
Type
journal article
Language
en
Open access
Licence
Locations
  • Respiratory Research (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, cc-by)
Funders
British Heart Foundation
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
  • Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
Keywords
chronic obstructive pulmonary disease, skeletal muscle atrophy, vastus lateralis, fat-free mass index, gene expression profiling, p21, cell cycle arrest, muscle atrophy, aging, exercise limitation, CYR61, BEX2, PMP22, GADD45A, therapeutic target, muscle transcriptome
MeSH terms
Aged, Female, Genetic Markers, Humans, Male, Muscular Atrophy, RNA, Messenger, Blotting, Western, Case-Control Studies, Cell Cycle Proteins, Reverse Transcriptase Polymerase Chain Reaction, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, Pulmonary Disease, Chronic Obstructive, Adiposity, Cyclin-Dependent Kinase Inhibitor p21, Quadriceps Muscle, Genome-Wide Association Study, Transcriptome

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