Table II.
Change | Pathway | Protein | Function |
---|---|---|---|
Proteins that increased | Hemostasis | C1QTNF1 | Suppresses platelet activation and aggregation; stimulates aldosterone secretion. |
vWF | Maintains hemostasis; promotes adhesion of platelets to sites of vascular injury by forming molecular bridges between subendothelial collagen matrix and platelet–surface receptor complex. | ||
Growth factor | FGF-19 | Suppresses bile acid biosynthesis; stimulates glucose uptake in adipocytes; member of heparin-binding growth factor family of proteins. | |
Immune regulation | GZMA | Protease that mediates pyroptosis and targets cell death by cytotoxic T cells and NK cells. | |
GZMB | Protease that mediates pyroptosis and targets cell death by cytotoxic T cells and NK cells; thought to be involved in the pathogenesis of COPD. | ||
GZMH | Cytotoxic chymotrypsin-like serine protease; probably necessary for target cell lysis in cell-mediated immune responses. | ||
IL-16 | Cytokine-mediated immune response: stimulates migratory response in CD4+ lymphocytes, monocytes, and eosinophils. | ||
KIR3DL1 | Role in regulation of immune response (NK cell–mediated cytotoxicity). | ||
DNA damage/repair | NBN | DNA integrity and genomic stability; component of MRE11-RAD50-NBN complex, which plays a crucial role in cellular response to DNA damage and maintenance of chromosome integrity. | |
PARP-1 | Poly-ADP-ribosyl transferase with key role in DNA repair and methylation. | ||
Protein that decreased | Growth factor | SPON2 | Cell adhesion protein; essential in initiation of innate immune response; represents unique pattern-recognition molecule for microbial pathogens. |
Threshold for statistically significant changes was P < .001. C1QTNF1, Complement C1q TNF-related protein 1; COPD, Chronic obstructive pulmonary disease; FGF-19, fibroblast growth factor 19; GZMA/B/H, granzyme A/B/H; KIR3DL1, killer cell immunoglobulin-like receptor 3DL1; NBN, nibrin; SPON2, spondin-2; vWF, von Willebrand factor.