Abstract
Chronic Obstructive Pulmonary Disease (COPD) affects 15.7 million Americans. Skeletal muscle dysfunction is a frequent comorbidity of COPD, which associates with worse prognosis including higher mortality and hospitalization rates, independently of the level of pulmonary disease. Moreover, recovery of skeletal muscle integrity in the context of rehabilitation exercises is associated with improved outcomes. To better understand the mechanisms underlying muscle wasting in COPD patients, a mouse model conditionally over expressing interleukin 13 (IL‐13+) in pulmonary Club cells has been developed. This animal demonstrates a pattern on skeletal muscle wasting that is highly reminiscent of the human counterpart. A comprehensive mass spectrometry‐based proteomics study demonstrated differences in skeletal muscle protein expression in wild type versus IL‐13+ mice. In this study, we used plasma samples to interrogate the proteomic profile of the wild type versus the IL‐13+ mice. Our hypothesis is that the proteomic signature found in skeletal muscle will, to some extent, overlap the pattern present in the plasma from the same animals indicating a systemic readout of skeletal muscle dysfunction. If our hypothesis is confirmed, we plan further validation studies using human plasma samples, which could facilitate early detection and potential interventions to ameliorate this devastating condition and have a significant impact on patients' outcomes.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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