Vis enkel innførsel

dc.contributor.authorOlsen, Maria Belland
dc.contributor.authorHildrestrand, Gunn Annette
dc.contributor.authorScheffler, Katja
dc.contributor.authorVinge, Leif Erik
dc.contributor.authorAlfsnes, Katrine
dc.contributor.authorPalibrk, Vuk
dc.contributor.authorWang, Junbai
dc.contributor.authorNeurauter, Christine Gran
dc.contributor.authorGomez, Luisa Fernanda Luna
dc.contributor.authorJohansen, Jostein
dc.contributor.authorØgaard, Jonas
dc.contributor.authorOhm, Ingrid Kristine
dc.contributor.authorSlupphaug, Geir
dc.contributor.authorKusnierczyk, Anna
dc.contributor.authorFiane, Arnt E
dc.contributor.authorBrorson, Sverre Henning
dc.contributor.authorZhang, Lili
dc.contributor.authorGullestad, Lars
dc.contributor.authorLouch, William Edward
dc.contributor.authorIversen, Per Ole
dc.contributor.authorØstlie, Ingunn
dc.contributor.authorKlungland, Arne
dc.contributor.authorChristensen, Geir Arve
dc.contributor.authorSjaastad, Ivar
dc.contributor.authorSætrom, Pål
dc.contributor.authorYndestad, Arne
dc.contributor.authorAukrust, Pål
dc.contributor.authorBjørås, Magnar
dc.contributor.authorFinsen, Alexandra
dc.identifier.citationCell reports. 2017, 18, 82-92.nb_NO
dc.description.abstractMyocardial infarction (MI) triggers a reparative response involving fibroblast proliferation and differentiation driving extracellular matrix modulation necessary to form a stabilizing scar. Recently, it was shown that a genetic variant of the base excision repair enzyme NEIL3 was associated with increased risk of MI in humans. Here, we report elevated myocardial NEIL3 expression in heart failure patients and marked myocardial upregulation of Neil3 after MI in mice, especially in a fibroblast-enriched cell fraction. Neil3−/− mice show increased mortality after MI caused by myocardial rupture. Genome-wide analysis of 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC) reveals changes in the cardiac epigenome, including in genes related to the post-MI transcriptional response. Differentially methylated genes are enriched in pathways related to proliferation and myofibroblast differentiation. Accordingly, Neil3−/− ruptured hearts show increased proliferation of fibroblasts and myofibroblasts. We propose that NEIL3-dependent modulation of DNA methylation regulates cardiac fibroblast proliferation and thereby affects extracellular matrix modulation after MI.nb_NO
dc.publisherCell Pressnb_NO
dc.rightsNavngivelse 4.0 Internasjonal*
dc.titleNEIL3-Dependent Regulation of Cardiac Fibroblast Proliferation Prevents Myocardial Rupturenb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.source.journalCell reportsnb_NO
dc.description.localcode© 2017 The Authors. This is an open access article under the CC BY license (
cristin.unitnameInstitutt for klinisk og molekylær medisin
cristin.unitnameInstitutt for datateknologi og informatikk

Tilhørende fil(er)


Denne innførselen finnes i følgende samling(er)

Vis enkel innførsel

Navngivelse 4.0 Internasjonal
Med mindre annet er angitt, så er denne innførselen lisensiert som Navngivelse 4.0 Internasjonal