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Neil3-dependent base excision repair regulates lipid metabolism and prevents atherosclerosis in Apoe-deficient mice

Skarpengland, T (author)
Holm, S (author)
Scheffler, K (author)
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Gregersen, I (author)
Dahl, TB (author)
Suganthan, R (author)
Segers, FM (author)
Ostlie, I (author)
Otten, JJT (author)
Luna, L (author)
Ketelhuth, DFJ (author)
Karolinska Institutet
Lundberg, AM (author)
Neurauter, CG (author)
Hildrestrand, G (author)
Skjelland, M (author)
Bjorndal, B (author)
Svardal, AM (author)
Iversen, PO (author)
Hedin, U (author)
Karolinska Institutet
Nygard, S (author)
Olstad, OK (author)
Krohg-Sorensen, K (author)
Slupphaug, G (author)
Eide, L (author)
Kusnierczyk, A (author)
Folkersen, L (author)
Ueland, T (author)
Berge, RK (author)
Hansson, GK (author)
Karolinska Institutet
Biessen, EAL (author)
Halvorsen, B (author)
Bjoras, M (author)
Aukrust, P (author)
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 (creator_code:org_t)
2016-06-22
2016
English.
In: Scientific reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 6, s. 28337-
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • 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.

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