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Tytuł pozycji:

Alterations in the sputum proteome and transcriptome in smokers and early-stage COPD subjects.

Tytuł :
Alterations in the sputum proteome and transcriptome in smokers and early-stage COPD subjects.
Autorzy :
Titz B; Philip Morris International R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, 2000 Neuchâtel, Switzerland. Electronic address: .
Sewer A; Philip Morris International R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, 2000 Neuchâtel, Switzerland.
Schneider T; Philip Morris International R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, 2000 Neuchâtel, Switzerland.
Elamin A; Philip Morris International R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, 2000 Neuchâtel, Switzerland.
Martin F; Philip Morris International R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, 2000 Neuchâtel, Switzerland.
Dijon S; Philip Morris International R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, 2000 Neuchâtel, Switzerland.
Luettich K; Philip Morris International R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, 2000 Neuchâtel, Switzerland.
Guedj E; Philip Morris International R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, 2000 Neuchâtel, Switzerland.
Vuillaume G; Philip Morris International R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, 2000 Neuchâtel, Switzerland.
Ivanov NV; Philip Morris International R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, 2000 Neuchâtel, Switzerland.
Peck MJ; Philip Morris International R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, 2000 Neuchâtel, Switzerland.
Chaudhary NI; Philip Morris International R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, 2000 Neuchâtel, Switzerland.
Hoeng J; Philip Morris International R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, 2000 Neuchâtel, Switzerland.
Peitsch MC; Philip Morris International R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, 2000 Neuchâtel, Switzerland.
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Źródło :
Journal of proteomics [J Proteomics] 2015 Oct 14; Vol. 128, pp. 306-20. Date of Electronic Publication: 2015 Aug 22.
Typ publikacji :
Journal Article; Randomized Controlled Trial
Język :
English
Imprint Name(s) :
Original Publication: Amsterdam : Elsevier
MeSH Terms :
Proteome/*metabolism
Pulmonary Disease, Chronic Obstructive/*metabolism
Smoking/*epidemiology
Smoking/*metabolism
Sputum/*metabolism
Transcription Factors/*metabolism
Adult ; Aged ; Biomarkers/blood ; Biomarkers/metabolism ; Causality ; Comorbidity ; Female ; Humans ; Male ; Middle Aged ; Prevalence ; Pulmonary Disease, Chronic Obstructive/diagnosis ; Pulmonary Disease, Chronic Obstructive/epidemiology ; Reproducibility of Results ; Risk Factors ; Sensitivity and Specificity ; Smoking Cessation/statistics & numerical data ; Smoking Prevention ; Transcriptome ; United Kingdom/epidemiology
Contributed Indexing :
Keywords: COPD; Quantitative proteomics; Smoking; Sputum; Systems toxicology
Substance Nomenclature :
0 (Biomarkers)
0 (Proteome)
0 (Transcription Factors)
Entry Date(s) :
Date Created: 20150827 Date Completed: 20160902 Latest Revision: 20171116
Update Code :
20201218
DOI :
10.1016/j.jprot.2015.08.009
PMID :
26306861
Czasopismo naukowe
Chronic obstructive pulmonary disease (COPD) is one of the most prevalent lung diseases. Cigarette smoking is the main risk factor for COPD. In this parallel-group clinical study we investigated to what extent the transitions in a chronic-exposure-to-disease model are reflected in the proteome and cellular transcriptome of induced sputum samples. We selected 60 age- and gender-matched individuals for each of the four study groups: current asymptomatic smokers, smokers with early stage COPD, former smokers, and never smokers. The cell-free sputum supernatant was analyzed by quantitative proteomics and the cellular mRNA fraction by gene expression profiling. The sputum proteome of current smokers clearly reflected the common physiological responses to smoke exposure, including alterations in mucin/trefoil proteins and a prominent xenobiotic/oxidative stress response. The latter response also was observed in the transcriptome, which additionally demonstrated an immune-cell polarization change. The former smoker group showed nearly complete attenuation of these biological effects. Thirteen differentially abundant proteins between the COPD and the asymptomatic smoker group were identified including TIMP1, APOA1, C6orf58, and BPIFB1 (LPLUNC1). In summary, our study demonstrates that sputum profiling can capture the complex and reversible physiological response to cigarette smoke exposure, which appears to be only slightly modulated in early-stage COPD.
(Copyright © 2015. Published by Elsevier B.V.)

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