Long-term impact of maternal high-fat diet on offspring cardiac health: role of micro-RNA biogenesis.
Journal
Cell death discovery
ISSN: 2058-7716
Titre abrégé: Cell Death Discov
Pays: United States
ID NLM: 101665035
Informations de publication
Date de publication:
2019
2019
Historique:
received:
03
01
2019
revised:
08
02
2019
accepted:
13
02
2019
entrez:
12
3
2019
pubmed:
12
3
2019
medline:
12
3
2019
Statut:
epublish
Résumé
Heart failure is a worldwide leading cause of death. Diet and obesity are particularly of high concern in heart disease etiology. Gravely, altered nutrition during developmental windows of vulnerability can have long-term impact on heart health; however, the underlying mechanisms are poorly understood. In the understanding of the initiation of chronic diseases related to developmental exposure to environmental challenges, deregulations in epigenetic mechanisms including micro-RNAs have been proposed as key events. In this context, we aimed at delineating the role of micro-RNAs in the programming of cardiac alterations induced by early developmental exposure to nutritional imbalance. To reach our aim, we developed a human relevant model of developmental exposure to nutritional imbalance by maternally exposing rat to high-fat diet during gestation and lactation. In this model, offspring exposed to maternal high-fat diet developed cardiac hypertrophy and increased extracellular matrix depot compared to those exposed to chow diet. Microarray approach performed on cardiac tissue allowed the identification of a micro-RNA subset which was down-regulated in high-fat diet-exposed animals and which were predicted to regulate transforming growth factor-beta (TGFβ)-mediated remodeling. As indicated by in vitro approaches and gene expression measurement in the heart of our animals, decrease in DiGeorge critical region 8 (DGCR8) expression, involved in micro-RNA biogenesis, seems to be a critical point in the alterations of the micro-RNA profile and the TGFβ-mediated remodeling induced by maternal exposure to high-fat diet. Finally, increasing DGCR8 activity and/or expression through hemin treatment in vitro revealed its potential in the rescue of the pro-fibrotic phenotype in cardiomyocytes driven by DGCR8 decrease. These findings suggest that cardiac alterations induced by maternal exposure to high-fat diet is related to abnormalities in TGFβ pathway and associated with down-regulated micro-RNA processing. Our study highlighted DGCR8 as a potential therapeutic target for heart diseases related to early exposure to dietary challenge.
Identifiants
pubmed: 30854230
doi: 10.1038/s41420-019-0153-y
pii: 153
pmc: PMC6397280
doi:
Types de publication
Journal Article
Langues
eng
Pagination
71Déclaration de conflit d'intérêts
The authors declare that they have no conflict of interest.
Références
Genet Couns. 1999;10(1):25-33
pubmed: 10191426
Proc Natl Acad Sci U S A. 2001 Oct 9;98(21):12283-8
pubmed: 11593045
Biochem Biophys Res Commun. 2003 Apr 25;304(1):184-90
pubmed: 12705904
Genes Dev. 2003 Dec 15;17(24):3011-6
pubmed: 14681208
Genes Dev. 2004 Dec 15;18(24):3016-27
pubmed: 15574589
Genes Dev. 2005 Dec 15;19(24):2979-90
pubmed: 16357216
Science. 2006 Apr 7;312(5770):117-21
pubmed: 16601194
Nat Struct Mol Biol. 2007 Jan;14(1):23-9
pubmed: 17159994
Cell Cycle. 2007 Jun 15;6(12):1426-31
pubmed: 17582223
Proc Natl Acad Sci U S A. 2008 Feb 12;105(6):2111-6
pubmed: 18256189
Toxicol Sci. 2008 Jun;103(2):228-40
pubmed: 18281715
Nat Genet. 2008 Jun;40(6):751-60
pubmed: 18469815
Nutr Rev. 2008 Aug;66(8):477-82
pubmed: 18667010
J Nutr. 2008 Sep;138(9):1622-7
pubmed: 18716160
Biol Reprod. 2008 Dec;79(6):1030-7
pubmed: 18716288
Circulation. 2008 Oct 7;118(15):1567-76
pubmed: 18809798
FASEB J. 2009 Mar;23(3):806-12
pubmed: 18952709
Genome Res. 2009 Jan;19(1):92-105
pubmed: 18955434
RNA. 2009 Mar;15(3):493-501
pubmed: 19176604
Circ Res. 2009 Sep 11;105(6):585-94
pubmed: 19679836
Mol Psychiatry. 2010 Dec;15(12):1176-89
pubmed: 19721432
Nat Rev Neurosci. 2010 Jun;11(6):402-16
pubmed: 20485365
J Mol Cell Cardiol. 2011 Oct;51(4):600-6
pubmed: 21059352
Cardiovasc Res. 2011 Jul 15;91(2):320-9
pubmed: 21406596
J Biol Chem. 2011 May 13;286(19):16716-25
pubmed: 21454614
Mol Cell Endocrinol. 2011 Jun 6;339(1-2):180-9
pubmed: 21550381
Lancet. 2011 May 21;377(9779):1760-9
pubmed: 21571362
EMBO Rep. 2012 Feb 01;13(2):142-9
pubmed: 22222205
Ageing Res Rev. 2012 Sep;11(4):491-500
pubmed: 22306790
Proc Natl Acad Sci U S A. 2012 Feb 7;109(6):1919-24
pubmed: 22308374
Protein Sci. 2012 Jun;21(6):797-808
pubmed: 22434730
Nucleic Acids Res. 2012 Jul;40(Web Server issue):W498-504
pubmed: 22649059
PLoS One. 2013 May 31;8(5):e66282
pubmed: 23741528
Physiol Genomics. 2013 Oct 1;45(19):889-900
pubmed: 23922128
BMJ. 2013 Aug 13;347:f4539
pubmed: 23943697
Cell Rep. 2013 Nov 27;5(4):1070-81
pubmed: 24239349
J Clin Invest. 2014 Jan;124(1):448-60
pubmed: 24355923
Proc Natl Acad Sci U S A. 2014 Feb 4;111(5):1861-6
pubmed: 24449907
Mutat Res Genet Toxicol Environ Mutagen. 2014 Apr;764-765:46-57
pubmed: 24486656
Endocrinology. 2014 Oct;155(10):3970-80
pubmed: 25051449
Mol Cell. 2015 Feb 5;57(3):397-407
pubmed: 25557550
BMC Nephrol. 2015 Apr 14;16:55
pubmed: 25881298
Chem Biol. 2015 Jun 18;22(6):793-802
pubmed: 26091172
Epigenomics. 2016 Nov;8(11):1459-1479
pubmed: 27762633
Microrna. 2017;6(1):2-16
pubmed: 27928946
Int J Mol Med. 2017 Aug;40(2):411-417
pubmed: 28627599
Card Fail Rev. 2017 Apr;3(1):7-11
pubmed: 28785469
Clin Chem. 2018 Jan;64(1):99-107
pubmed: 29158251
Cardiovasc Pathol. 2018 Jan - Feb;32:44-49
pubmed: 29198452
Nutr Metab Cardiovasc Dis. 2018 Jun;28(6):600-609
pubmed: 29691147
Nucleic Acids Res. 2018 Jun 20;46(11):5726-5736
pubmed: 29750274
Nutr Metab Cardiovasc Dis. 2018 Sep;28(9):944-951
pubmed: 29752038
J Dev Orig Health Dis. 2018 Dec;9(6):615-631
pubmed: 29909803
Cell. 1993 Jul 2;73(7):1435-44
pubmed: 8391934