dc.contributor.author | Skarpengland, Tonje | |
dc.contributor.author | Holm, Sverre | |
dc.contributor.author | Scheffler, Katja | |
dc.contributor.author | Gregersen, Ida | |
dc.contributor.author | Dahl, Tuva Børresdatter | |
dc.contributor.author | Suganthan, Rajikala | |
dc.contributor.author | Segers, Filip | |
dc.contributor.author | Østlie, Ingunn | |
dc.contributor.author | Otten, Jeroen J.T. | |
dc.contributor.author | Gomez, Luisa Fernanda Luna | |
dc.contributor.author | Ketelhuth, Daniel F.J. | |
dc.contributor.author | Lundberg, Anna M. | |
dc.contributor.author | Neurauter, Christine Gran | |
dc.contributor.author | Hildrestrand, Gunn Annette | |
dc.contributor.author | Skjelland, Mona | |
dc.contributor.author | Bjørndal, Bodil | |
dc.contributor.author | Svardal, Asbjørn M. | |
dc.contributor.author | Iversen, Per Ole | |
dc.contributor.author | Hedin, Ulf | |
dc.contributor.author | Nygård, Ståle | |
dc.contributor.author | Olstad, Ole Kristoffer | |
dc.contributor.author | Krohg-Sørensen, Kirsten | |
dc.contributor.author | Slupphaug, Geir | |
dc.contributor.author | Eide, Lars | |
dc.contributor.author | Kusnierczyk, Anna | |
dc.contributor.author | Folkersen, Lasse | |
dc.contributor.author | Ueland, Thor | |
dc.contributor.author | Berge, Rolf Kristian | |
dc.contributor.author | Hansson, Göran K. | |
dc.contributor.author | Biessen, Erik A.L. | |
dc.contributor.author | Halvorsen, Bente | |
dc.contributor.author | Bjørås, Magnar | |
dc.contributor.author | Aukrust, Pål | |
dc.date.accessioned | 2021-04-15T08:04:03Z | |
dc.date.available | 2021-04-15T08:04:03Z | |
dc.date.created | 2016-08-10T11:41:45Z | |
dc.date.issued | 2016 | |
dc.identifier.issn | 2045-2322 | |
dc.identifier.uri | https://hdl.handle.net/11250/2737856 | |
dc.description.abstract | Increasing 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.language.iso | eng | en_US |
dc.publisher | Nature Research | |
dc.rights | Navngivelse 4.0 Internasjonal | * |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/deed.no | * |
dc.title | Neil3-dependent base excision repair regulates lipid metabolism and prevents atherosclerosis in Apoe-deficient mice | en_US |
dc.type | Journal article | en_US |
dc.type | Peer reviewed | en_US |
dc.description.version | publishedVersion | en_US |
dc.source.articlenumber | 28337 | en_US |
cristin.ispublished | true | |
cristin.fulltext | original | |
cristin.qualitycode | 1 | |
dc.identifier.doi | 10.1038/srep28337 | |
dc.identifier.cristin | 1371776 | |
dc.source.journal | Scientific Reports | en_US |
dc.source.40 | 6:28337 | |
dc.identifier.citation | Scientific Reports. 2016, 6, 28337. | en_US |
dc.source.volume | 6 | en_US |