The matrikine acetyl-proline-glycine-proline and clinical features of COPD: findings from SPIROMICS.
Acetyl proline-glycine-proline (AcPGP)
Biomarker
COPD
Inflammation
Matrikine
Sputum
Journal
Respiratory research
ISSN: 1465-993X
Titre abrégé: Respir Res
Pays: England
ID NLM: 101090633
Informations de publication
Date de publication:
12 Nov 2019
12 Nov 2019
Historique:
received:
13
06
2019
accepted:
01
11
2019
entrez:
14
11
2019
pubmed:
14
11
2019
medline:
30
4
2020
Statut:
epublish
Résumé
Pulmonary and systemic inflammation are central features of chronic obstructive pulmonary disease (COPD). Previous studies have demonstrated relationships between biologically active extracellular matrix components, or matrikines, and COPD pathogenesis. We studied the relationships between the matrikine acetyl-proline-glycine-proline (AcPGP) in sputum and plasma and clinical features of COPD. Sputum and plasma samples were obtained from COPD participants in the SPIROMICS cohort at enrollment. AcPGP was isolated using solid phase extraction and measured by mass spectrometry. Demographics, spirometry, quality of life questionnaires, and quantitative computed tomography (CT) imaging with parametric response mapping (PRM) were obtained at baseline. Severe COPD exacerbations were recorded at 1-year of prospective follow-up. We used linear and logistic regression models to measure associations between AcPGP and features of COPD, and Kaplan-Meier analyses to measure time-to-first severe exacerbation. The 182 COPD participants in the analysis were 66 ± 8 years old, 62% male, 84% White race, and 39% were current smokers. AcPGP concentrations were 0.61 ± 1.89 ng/mL (mean ± SD) in sputum and 0.60 ± 1.13 ng/mL in plasma. In adjusted linear regression models, sputum AcPGP was associated with FEV In COPD, sputum but not plasma AcPGP concentrations are associated with the severity of airflow limitation, small airways disease, emphysema, and risk for severe AECOPD at 1-year of follow-up. ClinicalTrials.gov: NCT01969344 (SPIROMICS).
Sections du résumé
BACKGROUND
BACKGROUND
Pulmonary and systemic inflammation are central features of chronic obstructive pulmonary disease (COPD). Previous studies have demonstrated relationships between biologically active extracellular matrix components, or matrikines, and COPD pathogenesis. We studied the relationships between the matrikine acetyl-proline-glycine-proline (AcPGP) in sputum and plasma and clinical features of COPD.
METHODS
METHODS
Sputum and plasma samples were obtained from COPD participants in the SPIROMICS cohort at enrollment. AcPGP was isolated using solid phase extraction and measured by mass spectrometry. Demographics, spirometry, quality of life questionnaires, and quantitative computed tomography (CT) imaging with parametric response mapping (PRM) were obtained at baseline. Severe COPD exacerbations were recorded at 1-year of prospective follow-up. We used linear and logistic regression models to measure associations between AcPGP and features of COPD, and Kaplan-Meier analyses to measure time-to-first severe exacerbation.
RESULTS
RESULTS
The 182 COPD participants in the analysis were 66 ± 8 years old, 62% male, 84% White race, and 39% were current smokers. AcPGP concentrations were 0.61 ± 1.89 ng/mL (mean ± SD) in sputum and 0.60 ± 1.13 ng/mL in plasma. In adjusted linear regression models, sputum AcPGP was associated with FEV
CONCLUSIONS
CONCLUSIONS
In COPD, sputum but not plasma AcPGP concentrations are associated with the severity of airflow limitation, small airways disease, emphysema, and risk for severe AECOPD at 1-year of follow-up.
TRIAL REGISTRATION
BACKGROUND
ClinicalTrials.gov: NCT01969344 (SPIROMICS).
Identifiants
pubmed: 31718676
doi: 10.1186/s12931-019-1230-8
pii: 10.1186/s12931-019-1230-8
pmc: PMC6852714
doi:
Substances chimiques
Biomarkers
0
Proline
9DLQ4CIU6V
Glycine
TE7660XO1C
Banques de données
ClinicalTrials.gov
['NCT01969344']
Types de publication
Clinical Trial
Journal Article
Multicenter Study
Observational Study
Langues
eng
Sous-ensembles de citation
IM
Pagination
254Subventions
Organisme : NHLBI NIH HHS
ID : U24 HL141762
Pays : United States
Organisme : NIH HHS
ID : S10 OD018526
Pays : United States
Organisme : NIEHS NIH HHS
ID : P30 ES005605
Pays : United States
Organisme : U.S. Department of Veterans Affairs
ID : I01BX001756
Organisme : NHLBI NIH HHS
ID : K24 HL140108
Pays : United States
Organisme : NHLBI NIH HHS
ID : K08 HL123940
Pays : United States
Organisme : CSRD VA
ID : I01 CX000911
Pays : United States
Organisme : National Heart, Lung, and Blood Institute (US)
ID : HHSN268200900013C, HHSN268200900014C, HHSN268200900015C, HHSN268200900016C, HHSN268200900017C, HHSN268200900018C, HHSN268200900019C, HHSN268200900020C, U01 HL137880
Organisme : NHLBI NIH HHS
ID : R01 HL102371
Pays : United States
Organisme : NHLBI NIH HHS
ID : K24 HL137013
Pays : United States
Organisme : NHLBI NIH HHS
ID : U01 HL137880
Pays : United States
Organisme : NHLBI NIH HHS
ID : R35 HL135710
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK054759
Pays : United States
Organisme : National Heart, Lung, and Blood Institute (US)
ID : R01HL114439, R01HL126596,and R35HL135710
Investigateurs
Neil E Alexis
(NE)
Wayne H Anderson
(WH)
R Graham Barr
(RG)
Eugene R Bleecker
(ER)
Richard C Boucher
(RC)
Russell P Bowler
(RP)
Elizabeth E Carretta
(EE)
Stephanie A Christenson
(SA)
Alejandro P Comellas
(AP)
Christopher B Cooper
(CB)
David J Couper
(DJ)
Gerard J Criner
(GJ)
Ronald G Crystal
(RG)
Jeffrey L Curtis
(JL)
Claire M Doerschuk
(CM)
Mark T Dransfield
(MT)
Christine M Freeman
(CM)
Mei Lan K Han
(MLK)
Nadia N Hansel
(NN)
Annette T Hastie
(AT)
Eric A Hoffman
(EA)
Robert J Kaner
(RJ)
Richard E Kanner
(RE)
Eric C Kleerup
(EC)
Jerry A Krishnan
(JA)
Lisa M LaVange
(LM)
Stephen C Lazarus
(SC)
Fernando J Martinez
(FJ)
Deborah A Meyers
(DA)
John D Newell
(JD)
Elizabeth C Oelsner
(EC)
Wanda K O'Neal
(WK)
Robert Paine
(R)
Nirupama Putcha
(N)
Stephen I Rennard
(SI)
Donald P Tashkin
(DP)
Mary Beth Scholand
(MB)
J Michael Wells
(JM)
Robert A Wise
(RA)
Prescott G Woodruff
(PG)
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