miR-125b/NRF2/HO-1 axis is involved in protection against oxidative stress of cystic fibrosis: A pilot study.
cystic fibrosis
cystic fibrosis transmembrane conductance regulator
heme oxygenase-1
microRNA-125b
oxidative stress
Journal
Experimental and therapeutic medicine
ISSN: 1792-0981
Titre abrégé: Exp Ther Med
Pays: Greece
ID NLM: 101531947
Informations de publication
Date de publication:
Jun 2021
Jun 2021
Historique:
received:
10
08
2020
accepted:
24
11
2020
entrez:
14
4
2021
pubmed:
15
4
2021
medline:
15
4
2021
Statut:
ppublish
Résumé
In the physiopathology of cystic fibrosis (CF), oxidative stress implications are recognized and widely accepted. The cystic fibrosis transmembrane conductance regulator (CFTR) defects disrupt the intracellular redox balance causing CF pathological hallmarks. Therefore, oxidative stress together with aberrant expression levels of detoxification genes and microRNAs (miRNAs/miRs) may be associated with clinical outcome. Using total RNA extracted from epithelial nasal cells, the present study analyzed the expression levels of oxidative stress genes and one miRNA using quantitative PCR in a representative number of patients with CF compared with in healthy individuals. The present pilot study revealed the existence of an association among CFTR, genes involved in the oxidative stress response and miR-125b. The observed downregulation of CFTR gene expression was accompanied by increased expression levels of Nuclear factor erythroid derived-2 like2 and its targets NAD(P)H:Quinone Oxidoreductase and glutathione S-transferase 1. Moreover, the expression levels of heme oxygenase-1 (HO-1) and miR-125b were positively correlated with a forced expiratory volume in 1 sec (FEV1) >60% in patients with CF with chronic
Identifiants
pubmed: 33850557
doi: 10.3892/etm.2021.10017
pii: ETM-0-0-10017
pmc: PMC8027740
doi:
Types de publication
Journal Article
Langues
eng
Pagination
585Informations de copyright
Copyright © 2021, Spandidos Publications.
Déclaration de conflit d'intérêts
The authors declare that they have no competing interests.
Références
J Clin Invest. 1999 Jan;103(1):129-35
pubmed: 9884342
Am J Respir Cell Mol Biol. 1999 Sep;21(3):428-35
pubmed: 10460761
Cell Cycle. 2014;13(13):2046-55
pubmed: 24801890
Am J Respir Crit Care Med. 2004 Sep 15;170(6):633-40
pubmed: 15184199
Leukemia. 2015 Dec;29(12):2442-5
pubmed: 25982911
Cell Res. 2012 Oct;22(10):1453-66
pubmed: 22664907
Exp Dermatol. 2011 Nov;20(11):932-7
pubmed: 21913998
Redox Biol. 2013 Feb 05;1:190-202
pubmed: 24024153
J Cyst Fibros. 2008 Jan;7(1):44-53
pubmed: 17553758
Curr Pharm Des. 2018;24(20):2283-2302
pubmed: 30019638
Am J Clin Nutr. 2009 Sep;90(3):477-84
pubmed: 19587087
Sci Rep. 2018 Sep 19;8(1):14047
pubmed: 30232373
Oxid Med Cell Longev. 2017;2017:2872156
pubmed: 29312474
Biochim Biophys Acta. 2012 May;1822(5):690-713
pubmed: 22226887
Curr Pharm Des. 2017;23(10):1465-1470
pubmed: 28088909
Neurol Res. 2018 Oct;40(10):828-837
pubmed: 29956588
J Immunol. 2010 Feb 15;184(4):1702-9
pubmed: 20083669
Am J Respir Cell Mol Biol. 2008 Nov;39(5):560-8
pubmed: 18483420
Cell Death Dis. 2013 Oct 31;4:e899
pubmed: 24176857
Int J Biochem Cell Biol. 2014 Jul;52:113-23
pubmed: 24657650
Biochim Biophys Acta. 2016 Nov;1863(11):2650-2657
pubmed: 27523793
Clin Genet. 2010 Apr;77(4):306-13
pubmed: 20132241
Genes Dev. 2006 Mar 1;20(5):515-24
pubmed: 16510870
Cell Biol Int. 2011 May;35(5):463-6
pubmed: 21476987
Front Pharmacol. 2018 Oct 26;9:1176
pubmed: 30416443
Mediators Inflamm. 2015;2015:529642
pubmed: 26185362
J Biol Chem. 2011 Apr 1;286(13):11604-15
pubmed: 21282106
FEBS J. 2011 May;278(10):1598-609
pubmed: 21395977
Cell Death Dis. 2017 Jul 20;8(7):e2942
pubmed: 28726779
J Cyst Fibros. 2013 Dec;12(6):797-802
pubmed: 23632450
Antioxid Redox Signal. 2017 Aug 20;27(6):363-377
pubmed: 28257621
Cell Death Differ. 2015 Apr;22(4):654-64
pubmed: 25323587