Show simple item record

dc.contributor.authorSkarpengland, Tonje
dc.contributor.authorHolm, Sverre
dc.contributor.authorScheffler, Katja
dc.contributor.authorGregersen, Ida
dc.contributor.authorDahl, Tuva Børresdatter
dc.contributor.authorSuganthan, Rajikala
dc.contributor.authorSegers, Filip
dc.contributor.authorØstlie, Ingunn
dc.contributor.authorOtten, Jeroen J.T.
dc.contributor.authorGomez, Luisa Fernanda Luna
dc.contributor.authorKetelhuth, Daniel F.J.
dc.contributor.authorLundberg, Anna M.
dc.contributor.authorNeurauter, Christine Gran
dc.contributor.authorHildrestrand, Gunn Annette
dc.contributor.authorSkjelland, Mona
dc.contributor.authorBjørndal, Bodil
dc.contributor.authorSvardal, Asbjørn M.
dc.contributor.authorIversen, Per Ole
dc.contributor.authorHedin, Ulf
dc.contributor.authorNygård, Ståle
dc.contributor.authorOlstad, Ole Kristoffer
dc.contributor.authorKrohg-Sørensen, Kirsten
dc.contributor.authorSlupphaug, Geir
dc.contributor.authorEide, Lars
dc.contributor.authorKusnierczyk, Anna
dc.contributor.authorFolkersen, Lasse
dc.contributor.authorUeland, Thor
dc.contributor.authorBerge, Rolf Kristian
dc.contributor.authorHansson, Göran K.
dc.contributor.authorBiessen, Erik A.L.
dc.contributor.authorHalvorsen, Bente
dc.contributor.authorBjørås, Magnar
dc.contributor.authorAukrust, Pål
dc.description.abstractIncreasing evidence suggests that oxidative DNA damage accumulates in atherosclerosis. Recently, we showed that a genetic variant in the human DNA repair enzyme NEIL3 was associated with increased risk of myocardial infarction. Here, we explored the role of Neil3/NEIL3 in atherogenesis by both clinical and experimental approaches. Human carotid plaques revealed increased NEIL3 mRNA expression which significantly correlated with mRNA levels of the macrophage marker CD68. Apoe−/−Neil3−/− mice on high-fat diet showed accelerated plaque formation as compared to Apoe−/− mice, reflecting an atherogenic lipid profile, increased hepatic triglyceride levels and attenuated macrophage cholesterol efflux capacity. Apoe−/−Neil3−/− mice showed marked alterations in several pathways affecting hepatic lipid metabolism, but no genotypic alterations in genome integrity or genome-wide accumulation of oxidative DNA damage. These results suggest a novel role for the DNA glycosylase Neil3 in atherogenesis in balancing lipid metabolism and macrophage function, potentially independently of genome-wide canonical base excision repair of oxidative DNA damage.en_US
dc.publisherNature Researchen_US
dc.rightsNavngivelse 4.0 Internasjonal*
dc.titleNeil3-dependent base excision repair regulates lipid metabolism and prevents atherosclerosis in Apoe-deficient miceen_US
dc.typePeer revieweden_US
dc.typeJournal articleen_US
dc.source.journalScientific Reportsen_US
dc.description.localcodeThis work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit

Files in this item


This item appears in the following Collection(s)

Show simple item record

Navngivelse 4.0 Internasjonal
Except where otherwise noted, this item's license is described as Navngivelse 4.0 Internasjonal