Analysis of the polarization states of the alveolar macrophages in chronic obstructive pulmonary disease samples based on miRNA-mRNA network signatures.
Chronic obstructive pulmonary disease (COPD)
macrophage cells
messenger RNA (mRNA)
microRNA (miRNA)
polarization states
Journal
Annals of translational medicine
ISSN: 2305-5839
Titre abrégé: Ann Transl Med
Pays: China
ID NLM: 101617978
Informations de publication
Date de publication:
Aug 2021
Aug 2021
Historique:
received:
02
07
2021
accepted:
12
08
2021
entrez:
17
9
2021
pubmed:
18
9
2021
medline:
18
9
2021
Statut:
ppublish
Résumé
Multiple gene expression studies have been performed to investigate the biomarkers of chronic obstructive pulmonary disease (COPD). However, few studies have related COPD to macrophage cells. The gene expression levels of clinical samples of COPD smokers (COPD; n=6), healthy smokers (Smoke; n=11), and never smokers (Never; n=4) were downloaded from the Gene Expression Omnibus (GEO) repository of GSE124180. The expression levels of messenger RNAs (mRNAs) and microRNAs (miRNAs) in macrophage cells of M0 (n=7), M1 (n=7), and M2 (n=7) were downloaded from the GEO repository of GSE46903 and GSE51307. Differentially expressed (DE) mRNAs (DEmRNAs) were identified by edgeR and GEO2R, with an adjusted P value <0.05 and |log The composition of macrophages was quite different between COPD, Never, and Smoke samples. The proportion of M1 cells was lower than that of M0 and M2 cells in Smokers and COPD samples. Most of the genes specifically up-regulated in M1 are related to inflammation/immunity. The expression levels of miR-30a-5p, miR-200c-3p, miR-20b-5p, miR-199b-5p, and miR-301b-3p in M1 macrophages were all lower than that of M0. Their expression levels in M2 macrophages compared with M1 varied, with higher expression in miR-30a-5p, miR-20b-5p, and lower expression in miR-200c-3p, and miR-301b-3p. The mRNAs of the fms related receptor tyrosine kinase 1 ( The present study mined the miRNA-mRNA signature which might play an essential role in COPD and macrophage polarization.
Sections du résumé
BACKGROUND
BACKGROUND
Multiple gene expression studies have been performed to investigate the biomarkers of chronic obstructive pulmonary disease (COPD). However, few studies have related COPD to macrophage cells.
METHODS
METHODS
The gene expression levels of clinical samples of COPD smokers (COPD; n=6), healthy smokers (Smoke; n=11), and never smokers (Never; n=4) were downloaded from the Gene Expression Omnibus (GEO) repository of GSE124180. The expression levels of messenger RNAs (mRNAs) and microRNAs (miRNAs) in macrophage cells of M0 (n=7), M1 (n=7), and M2 (n=7) were downloaded from the GEO repository of GSE46903 and GSE51307. Differentially expressed (DE) mRNAs (DEmRNAs) were identified by edgeR and GEO2R, with an adjusted P value <0.05 and |log
RESULTS
RESULTS
The composition of macrophages was quite different between COPD, Never, and Smoke samples. The proportion of M1 cells was lower than that of M0 and M2 cells in Smokers and COPD samples. Most of the genes specifically up-regulated in M1 are related to inflammation/immunity. The expression levels of miR-30a-5p, miR-200c-3p, miR-20b-5p, miR-199b-5p, and miR-301b-3p in M1 macrophages were all lower than that of M0. Their expression levels in M2 macrophages compared with M1 varied, with higher expression in miR-30a-5p, miR-20b-5p, and lower expression in miR-200c-3p, and miR-301b-3p. The mRNAs of the fms related receptor tyrosine kinase 1 (
CONCLUSIONS
CONCLUSIONS
The present study mined the miRNA-mRNA signature which might play an essential role in COPD and macrophage polarization.
Identifiants
pubmed: 34532470
doi: 10.21037/atm-21-3815
pii: atm-09-16-1333
pmc: PMC8422127
doi:
Types de publication
Journal Article
Langues
eng
Pagination
1333Informations de copyright
2021 Annals of Translational Medicine. All rights reserved.
Déclaration de conflit d'intérêts
Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://dx.doi.org/10.21037/atm-21-3815). The authors have no conflicts of interest to declare.
Références
Blood. 2001 Feb 1;97(3):785-91
pubmed: 11157498
BMC Med Genomics. 2017 Oct 6;10(1):58
pubmed: 28985737
Eur J Pharmacol. 2020 Jun 15;877:173090
pubmed: 32234529
Respir Res. 2019 Aug 9;20(1):180
pubmed: 31399091
Int J Mol Sci. 2020 Jan 28;21(3):
pubmed: 32013028
Am J Respir Cell Mol Biol. 2019 Apr;60(4):445-453
pubmed: 30395484
Respir Investig. 2014 Mar;52(2):92-100
pubmed: 24636264
J Immunol. 2009 Aug 15;183(4):2867-83
pubmed: 19635926
Front Immunol. 2018 Jul 19;9:1650
pubmed: 30072995
Int Immunopharmacol. 2019 Feb;67:335-347
pubmed: 30578969
Eur J Microbiol Immunol (Bp). 2012 Sep;2(3):176-85
pubmed: 24688763
J Pharmacol Exp Ther. 2019 Jun;369(3):473-480
pubmed: 30952680
Chest. 2014 Jul;146(1):193-204
pubmed: 25010962
BMC Pulm Med. 2018 Jun 15;18(1):101
pubmed: 29907106
Front Pharmacol. 2020 Mar 12;11:259
pubmed: 32226383
Am J Respir Crit Care Med. 2013 May 1;187(9):933-42
pubmed: 23471465
J Allergy Clin Immunol. 2016 Jul;138(1):16-27
pubmed: 27373322
Drugs. 2017 Apr;77(5):521-546
pubmed: 28255960
Mutagenesis. 2014 Sep;29(5):311-7
pubmed: 24891316
Cell Physiol Biochem. 2017;43(2):743-756
pubmed: 28950251
BMC Med Genomics. 2020 Sep 10;13(1):128
pubmed: 32912198
Biomed Res Int. 2021 Jun 20;2021:9921012
pubmed: 34250093
Ann Am Thorac Soc. 2013 Dec;10 Suppl:S180-5
pubmed: 24313770
Cytokine. 2019 Nov;123:154739
pubmed: 31319374
Mediators Inflamm. 2013;2013:413735
pubmed: 23956502
Am J Respir Crit Care Med. 2003 Oct 15;168(8):976-82
pubmed: 12816740
Oncogenesis. 2018 Oct 8;7(10):79
pubmed: 30293994
Eur Respir J. 2019 May 18;53(5):
pubmed: 30846476
Proc Am Thorac Soc. 2005;2(1):71-7
pubmed: 16113472
Am J Hum Genet. 2007 May;80(5):966-70
pubmed: 17436251
Prev Med. 2012 May;54 Suppl:S20-8
pubmed: 22178470
Eur Respir J. 2015 Apr;45(4):1150-62
pubmed: 25700381
Respir Res. 2011 Jan 27;12:18
pubmed: 21272339
Arterioscler Thromb Vasc Biol. 2000 Feb;20(2):377-84
pubmed: 10669633
Ann Rheum Dis. 2017 Jun;76(6):1133-1141
pubmed: 28209630
J Photochem Photobiol B. 2014 Jan 5;130:146-52
pubmed: 24333762
Nanomedicine. 2019 Jun;18:259-271
pubmed: 30981817
Lancet. 2015 Mar 7;385(9971):857-66
pubmed: 25684586
Proc Natl Acad Sci U S A. 2004 Jul 6;101(27):10143-8
pubmed: 15210990
Proc Natl Acad Sci U S A. 2004 Mar 30;101(13):4560-5
pubmed: 15070757
Thorax. 2005 Feb;60(2):106-13
pubmed: 15681497
Bioinformatics. 2010 Jan 1;26(1):139-40
pubmed: 19910308
Sci Rep. 2017 Mar 03;7:43315
pubmed: 28256556
Respir Res. 2019 Apr 2;20(1):65
pubmed: 30940135
Respir Res. 2017 Jan 5;18(1):4
pubmed: 28057018
BMC Pulm Med. 2018 Mar 5;18(1):42
pubmed: 29506519
Cell. 2009 Jan 23;136(2):215-33
pubmed: 19167326
Immunity. 2014 Feb 20;40(2):274-88
pubmed: 24530056
Int J Mol Sci. 2018 Feb 15;19(2):
pubmed: 29462886
PLoS One. 2017 Oct 9;12(10):e0185682
pubmed: 29016655
Acta Histochem. 2008;110(4):285-93
pubmed: 18321563
Int J Chron Obstruct Pulmon Dis. 2017 Jun 23;12:1811-1817
pubmed: 28694694
Hum Mol Genet. 2016 Nov 1;25(21):4611-4623
pubmed: 28158590
Chest. 2013 Jan;143(1):196-206
pubmed: 23276842
BMC Med Genomics. 2012 Dec 03;5:58
pubmed: 23210427
Respir Res. 2017 Apr 24;18(1):72
pubmed: 28438154
Proc Am Thorac Soc. 2009 Dec;6(8):697-700
pubmed: 20008878
Respir Res. 2017 Apr 18;18(1):61
pubmed: 28420398
FASEB J. 2019 Nov;33(11):12200-12212
pubmed: 31373848
Biomed Pharmacother. 2019 Sep;117:109015
pubmed: 31207576
PLoS One. 2011;6(7):e22798
pubmed: 21829517
Thorax. 2007 Dec;62(12):1081-7
pubmed: 17573446