Open Access Green: Postprint online verfügbar 11/2020 möglich sobald bei der ZB eingereicht worden ist.
Cigarette smoke induces overexpression of active human cathepsin S in lungs from current smokers with or without COPD.
Am. J. Physiol. Lung Cell Mol. Physiol. 317, L625-L638 (2019)
DOI Verlagsversion bestellen
Cigarette smoking has marked effects on lung tissue, including induction of oxidative stress, inflammatory cell recruitment, and a protease/antiprotease imbalance. These effects contribute to tissue remodeling and destruction resulting in loss of lung function in chronic obstructive pulmonary disease (COPD) patients. Cathepsin S (CatS) is a cysteine protease that is involved in the remodeling/degradation of connective tissue and basement membrane. Aberrant expression or activity of CatS has been implicated in a variety of diseases, including arthritis, cancer, cardiovascular, and lung diseases. However, little is known about the effect of cigarette smoking on both CatS expression and activity, as well as its role in smoking-related lung diseases. Here, we evaluated the expression and activity of human CatS in lung tissues from never-smokers and smokers with or without COPD. Despite the presence of an oxidizing environment, CatS expression and activity were significantly higher in current smokers (both non-COPD and COPD) compared with never-smokers, and correlated positively with smoking history. Moreover, we found that the exposure of primary human bronchial epithelial cells to cigarette smoke extract triggered the activation of P2X7 receptors, which in turns drives CatS upregulation. The present data suggest that excessive CatS expression and activity contribute, beside other proteases, to the deleterious effects of cigarette smoke on pulmonary homeostasis.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Cigarette Smoke ; Copd ; Cysteine Protease ; Oxidation ; Smokers; Cysteine Cathepsins; Emerging Roles; Expression; Release; Macrophages; Inhibitor; Emphysema; Pathogenesis; Mechanisms; Cessation
ISSN (print) / ISBN 1040-0605
Zeitschrift American Journal of Physiology - Lung Cellular and Molecular Physiology
Quellenangaben Band: 317, Heft: 5, Seiten: L625-L638
Verlag American Physiological Society
Verlagsort Bethesda, Md. [u.a.]
Institut(e) Institute of Lung Biology (ILBD)