Translation of genomic alterations to protein changes in chronic obstructive pulmonary disease (COPD) is largely unexplored. Using integrated proteomic and RNA sequencing analysis of COPD and control lung tissues, we identified a protein signature in COPD characterised by extracellular matrix changes and a potential regulatory role for SUMO2. Furthermore, we identified 61 differentially expressed novel, non-reference, peptides in COPD compared with control lungs. This included two peptides encoding for a new splice variant of SORBS1, of which the transcript usage was higher in COPD compared with control lungs. These explorative findings and integrative proteogenomic approach open new avenues to further unravel the pathology of COPD.
- COPD ÀÜ mechanisms
- COPD pathology
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C-AB and VG contributed equally.
MvdB and PH contributed equally.
Deceased Deceased: Thomas E Fehniger
Funding University Medical Center Groningen.
Competing interests WT reports personal fees from Pfizer, personal fees from GSK, personal fees from Chiesi, from Roche Diagnostics/Ventana, grants from Dutch Asthma Fund, personal fees from Biotest, personal fees from Merck Sharp Dohme, personal fees from Novartis, personal fees from Lilly Oncology, personal fees from Boehringer Ingelheim, personal fees from Astra-Zeneca, personal fees from Bristol-Myers-Squibb, all outside the submitted work. MvdB reports research grants paid to University from GlaxoSmithKline, TEVA and Chiesi, outside the submitted work. The University of Groningen received money from GSK and Chiesi for consultancy and travel by DSP, outside the submitted work. C-AB, VG, AC, RB, MJ, EO, JM, GM-V, TF and PH have nothing to disclose.
Patient consent for publication Not required.
Provenance and peer review Not commissioned; externally peer reviewed.
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