Premium
Use of Mass Spectrometry‐Based Proteomics to Investigate Protein Regulation Associated with COPD‐Related Muscle Dysfunction
Author(s) -
Schiltz Sarah B.,
Balnis Joseph,
Jaitovich Ariel,
Vincent Catherine E.
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.05256
Subject(s) - copd , skeletal muscle , hemopexin , wasting , proteomics , medicine , bioinformatics , sarcopenia , disease , biology , endocrinology , genetics , biochemistry , gene , heme , enzyme
Chronic Obstructive Pulmonary Disease (COPD) is an umbrella term used to encompass several progressive lung diseases. A common comorbidity of COPD is skeletal muscle dysfunction with muscle mass loss, a condition shown to decrease quality of life and increase mortality rates independently of the level of pulmonary disease. Interestingly, rehabilitation exercises for the recovery of skeletal muscle integrity has been associated with improved disease outcomes. There are two mouse models that have been developed to mimic the COPD phenotype and demonstrate skeletal muscle wasting that recapitulates the disease seen in humans. A comprehensive mass spectrometry‐based proteomics study in one of these models (a mouse conditionally over‐expressing interleukin‐13, IL13 TG ) yielded a set of potential protein biomarkers for the degree of muscle dysfunction in skeletal muscle, including haptoglobin, hemopexin, and ceruloplasmin. Our present study will use mass spectrometry‐based proteomics to interrogate protein regulation in the EDL muscle of the other mouse model (a mouse that has lung‐specific expression of human matrix metalloproteinase‐1 (MMP‐1), an interstitial collagenase). We hypothesize that we will find a set of regulated proteins in common between the two studies, providing a set of conclusive biomarkers for COPD‐related skeletal muscle dysfunction that are independent of genetic modification. If our hypothesis is confirmed, we will then have a list of potential targets that can help facilitate early detection and/or potential interventions for COPD in humans to achieve improved patient outcomes. Support or Funding Information Part of the results reported herein have been funded Hartwick College and by NHLBI of the National Institutes of Health under the award number K01‐HL130704 (AJ), and by the Collins Family Foundation Endowment (AJ); NIH/NHLBI 5R01HL049426 (HAS); NIH/NHLBI PO1 HL114501(JAE); R01 HL115813 (CGL); NIH/NIGMS grant 1R01GM124133 (APA)