Time-resolved proteomic profiling of cigarette smoke-induced experimental chronic obstructive pulmonary disease.

Skerrett-Byrne, DA; Bromfield, EG; Murray, HC; Jamaluddin, MFB; Jarnicki, AG; Fricker, M; Essilfie, AT; Jones, B; Haw, TJ; Hampsey, D; Anderson, AL; Nixon, B; Scott, RJ; Wark, PAB; Dun, MD; Hansbro, PM

Time-resolved proteomic profiling of cigarette smoke-induced experimental chronic obstructive pulmonary disease.

Skerrett-Byrne, DA Bromfield, EG Murray, HC Jamaluddin, MFB Jarnicki, AG Fricker, M Essilfie, AT Jones, B Haw, TJ Hampsey, D Anderson, AL Nixon, B Scott, RJ Wark, PAB Dun, MD Hansbro, PM

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Publisher:: Wiley
Publication Type:: Journal Article
Citation:: Respirology, 2021, 26, (10), pp. 960-973
Issue Date:: 2021-10

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	Respirology - 2021 - Skerrett%E2%80%90Byrne - Time%E2%80%90resolved proteomic profiling of cigarette smoke%E2%80%90induced experimental chronic.pdf	Published version	17.97 MB		View/Open

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Field	Value	Language
dc.contributor.author	Skerrett-Byrne, DA
dc.contributor.author	Bromfield, EG
dc.contributor.author	Murray, HC
dc.contributor.author	Jamaluddin, MFB
dc.contributor.author	Jarnicki, AG
dc.contributor.author	Fricker, M
dc.contributor.author	Essilfie, AT
dc.contributor.author	Jones, B
dc.contributor.author	Haw, TJ
dc.contributor.author	Hampsey, D
dc.contributor.author	Anderson, AL
dc.contributor.author	Nixon, B
dc.contributor.author	Scott, RJ
dc.contributor.author	Wark, PAB
dc.contributor.author	Dun, MD
dc.contributor.author	Hansbro, PM
dc.date.accessioned	2022-02-14T22:57:08Z
dc.date.available	2021-06-14
dc.date.available	2022-02-14T22:57:08Z
dc.date.issued	2021-10
dc.identifier.citation	Respirology, 2021, 26, (10), pp. 960-973
dc.identifier.issn	1323-7799
dc.identifier.issn	1440-1843
dc.identifier.uri	http://hdl.handle.net/10453/154511
dc.description.abstract	BACKGROUND AND OBJECTIVE: Chronic obstructive pulmonary disease (COPD) is the third leading cause of illness and death worldwide. Current treatments aim to control symptoms with none able to reverse disease or stop its progression. We explored the major molecular changes in COPD pathogenesis. METHODS: We employed quantitative label-based proteomics to map the changes in the lung tissue proteome of cigarette smoke-induced experimental COPD that is induced over 8 weeks and progresses over 12 weeks. RESULTS: Quantification of 7324 proteins enabled the tracking of changes to the proteome. Alterations in protein expression profiles occurred in the induction phase, with 18 and 16 protein changes at 4- and 6-week time points, compared to age-matched controls, respectively. Strikingly, 269 proteins had altered expression after 8 weeks when the hallmark pathological features of human COPD emerge, but this dropped to 27 changes at 12 weeks with disease progression. Differentially expressed proteins were validated using other mouse and human COPD bronchial biopsy samples. Major changes in RNA biosynthesis (heterogeneous nuclear ribonucleoproteins C1/C2 [HNRNPC] and RNA-binding protein Musashi homologue 2 [MSI2]) and modulators of inflammatory responses (S100A1) were notable. Mitochondrial dysfunction and changes in oxidative stress proteins also occurred. CONCLUSION: We provide a detailed proteomic profile, identifying proteins associated with the pathogenesis and disease progression of COPD establishing a platform to develop effective new treatment strategies.
dc.format	Print-Electronic
dc.language	eng
dc.publisher	Wiley
dc.relation	http://purl.org/au-research/grants/nhmrc/APP1079184
dc.relation	http://purl.org/au-research/grants/nhmrc/APP1156589
dc.relation	http://purl.org/au-research/grants/nhmrc/APP1099095
dc.relation	http://purl.org/au-research/grants/nhmrc/APP1137995
dc.relation	http://purl.org/au-research/grants/nhmrc/GNT1079187
dc.relation	http://purl.org/au-research/grants/nhmrc/1003593
dc.relation	http://purl.org/au-research/grants/nhmrc/1179092
dc.relation	http://purl.org/au-research/grants/nhmrc/1175134
dc.relation.ispartof	Respirology
dc.relation.isbasedon	10.1111/resp.14111
dc.rights	info:eu-repo/semantics/closedAccess
dc.subject	11 Medical and Health Sciences
dc.subject.classification	Respiratory System
dc.subject.mesh	Animals
dc.subject.mesh	Disease Models, Animal
dc.subject.mesh	Lung
dc.subject.mesh	Mice
dc.subject.mesh	Proteomics
dc.subject.mesh	Pulmonary Disease, Chronic Obstructive
dc.subject.mesh	Smoke
dc.subject.mesh	Smoking
dc.subject.mesh	Animals
dc.subject.mesh	Disease Models, Animal
dc.subject.mesh	Lung
dc.subject.mesh	Mice
dc.subject.mesh	Proteomics
dc.subject.mesh	Pulmonary Disease, Chronic Obstructive
dc.subject.mesh	Smoke
dc.subject.mesh	Smoking
dc.subject.mesh	Lung
dc.subject.mesh	Animals
dc.subject.mesh	Mice
dc.subject.mesh	Pulmonary Disease, Chronic Obstructive
dc.subject.mesh	Disease Models, Animal
dc.subject.mesh	Smoking
dc.subject.mesh	Proteomics
dc.subject.mesh	Smoke
dc.title	Time-resolved proteomic profiling of cigarette smoke-induced experimental chronic obstructive pulmonary disease.
dc.type	Journal Article
utslib.citation.volume	26
utslib.location.activity	Australia
utslib.for	11 Medical and Health Sciences
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
utslib.copyright.status	closed_access	*
pubs.consider-herdc	false
dc.date.updated	2022-02-14T22:57:00Z
pubs.issue	10
pubs.publication-status	Published
pubs.volume	26
utslib.citation.issue	10

Abstract:

BACKGROUND AND OBJECTIVE: Chronic obstructive pulmonary disease (COPD) is the third leading cause of illness and death worldwide. Current treatments aim to control symptoms with none able to reverse disease or stop its progression. We explored the major molecular changes in COPD pathogenesis. METHODS: We employed quantitative label-based proteomics to map the changes in the lung tissue proteome of cigarette smoke-induced experimental COPD that is induced over 8 weeks and progresses over 12 weeks. RESULTS: Quantification of 7324 proteins enabled the tracking of changes to the proteome. Alterations in protein expression profiles occurred in the induction phase, with 18 and 16 protein changes at 4- and 6-week time points, compared to age-matched controls, respectively. Strikingly, 269 proteins had altered expression after 8 weeks when the hallmark pathological features of human COPD emerge, but this dropped to 27 changes at 12 weeks with disease progression. Differentially expressed proteins were validated using other mouse and human COPD bronchial biopsy samples. Major changes in RNA biosynthesis (heterogeneous nuclear ribonucleoproteins C1/C2 [HNRNPC] and RNA-binding protein Musashi homologue 2 [MSI2]) and modulators of inflammatory responses (S100A1) were notable. Mitochondrial dysfunction and changes in oxidative stress proteins also occurred. CONCLUSION: We provide a detailed proteomic profile, identifying proteins associated with the pathogenesis and disease progression of COPD establishing a platform to develop effective new treatment strategies.

Please use this identifier to cite or link to this item:

http://hdl.handle.net/10453/154511