Proteomic profiling of COPD may lead to new treatment strategies

A recent study has provided a detailed proteomic profile that identified proteins associated with the pathogenesis and disease progression of chronic obstructive pulmonary disease (COPD), which can then help in the creation of platform to develop effective new treatment strategies.

The authors explored the major molecular changes in COPD pathogenesis and used quantitative label-based proteomics to map such changes in the lung tissue proteome of cigarette smoke-induced experimental COPD that was induced over 8 weeks and progressed over 12 weeks.

A total of 7,234 proteins were quantified, enabling the tracking of changes to the proteome. Changes in protein expression profiles occurred in the induction phase, with 18 and 16 protein alterations at weeks 4 and 6, respectively, compared to age-matched controls. At week 8, 269 proteins had altered expression when the hallmark pathological features of human COPD emerged. This decreased to 27 changes at 12 weeks with disease progression.

Other mouse and human COPD bronchial biopsy samples validated these altered protein expressions. Furthermore, there were major changes in RNA biosynthesis (heterogeneous nuclear ribonucleoproteins C1/C2 and RNA-binding protein Musashi homologue 2) and modulators of inflammatory responses (S100A1), as well as mitochondrial dysfunction and alterations in oxidative stress proteins.

“COPD is the third leading cause of illness and death worldwide,” the authors said. “Current treatments aim to control symptoms, with none [being] able to reverse disease or stop its progression.”