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Lars Eide
University of Oslo
DNA repairDNA damageMolecular biologyMitochondrial DNABiology
63Publications
20H-index
3,423Citations
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Publications 64
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#1Mingyi Yang (Oslo University Hospital)H-Index: 4
#1Mingyi Yang (Oslo University Hospital)
Last. Nils Bolstad (Oslo University Hospital)H-Index: 9
view all 21 authors...
Summary Oxidation resistance gene 1 (OXR1) protects cells against oxidative stress. We find that male mice with brain-specific isoform A knockout (Oxr1A−/−) develop fatty liver. RNA sequencing of male Oxr1A−/− liver indicates decreased growth hormone (GH) signaling, which is known to affect liver metabolism. Indeed, Gh expression is reduced in male mice Oxr1A−/− pituitary gland and in rat Oxr1A−/− pituitary adenoma cell-line GH3. Oxr1A−/− male mice show reduced fasting-blood GH levels. Pull-down...
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#1Marie Rodinova (First Faculty of Medicine, Charles University in Prague)H-Index: 2
#2Jana Krizova (First Faculty of Medicine, Charles University in Prague)H-Index: 1
Last. Hana Hansikova (First Faculty of Medicine, Charles University in Prague)H-Index: 14
view all 13 authors...
ABSTRACT Skeletal muscle wasting and atrophy is one of the more severe clinical impairments resulting from the progression of Huntington9s disease (HD). Mitochondrial dysfunction may play a significant role in the etiology of HD, but the specific condition of mitochondria in muscle has not been widely studied during the development of HD. To determine the role of mitochondria in skeletal muscle during the early stages of HD, we analyzed quadriceps femoris muscle from 24-, 36-, 48- and 66-month-o...
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Background: Huntington’s disease (HD) is a devastating neurodegenerative disorder caused by CAG triplet expansions in the huntingtin gene. Oxidative stress is linked to HD pathology, although it is not clear whether this is an effect or a mediator of disease. The transgenic (TgHD) minipig expresses the N-terminal part of human-mutated huntingtin and represents a unique model to investigate therapeutic strategies towards HD. A more detailed characterization of this model is needed to fully utiliz...
1 CitationsSource
#1Paula A. Bousquet (Ahus: Akershus University Hospital)H-Index: 1
#2Sebastian Meltzer (University of Oslo)H-Index: 4
Last. Anne Hansen Ree (University of Oslo)H-Index: 24
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Abstract Tumor hypoxia contributes to therapy resistance and metastatic progression of locally advanced rectal cancer (LARC). We postulated that the tumor mitochondrial metabolism, manifested by reactive oxygen species (ROS) and mitochondrial DNA (mtDNA) damage, reflects how hypoxic conditions connect to cancer-induced systemic inflammation and poor outcome. Levels of ROS and mtDNA damage were analyzed in three colorectal cancer (CRC) cell lines cultured for 24 hours under normoxia (21% O2) or h...
2 CitationsSource
#1Georgina Askeland (University of Oslo)H-Index: 2
#2Marie Rodinova (Charles University in Prague)H-Index: 2
Last. Lars Eide (University of Oslo)H-Index: 20
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ABSTRACT Huntington9s disease (HD) is a monogenic, progressive, neurodegenerative disorder with currently no available treatment. The Libechov transgenic minipig model for HD (TgHD) displays neuroanatomical similarities to humans and exhibits slow disease progression, and is therefore more powerful than available mouse models for the development of therapy. The phenotypic characterization of this model is still ongoing, and it is essential to validate biomarkers to monitor disease progression an...
3 CitationsSource
#1Petra SmatlikovaH-Index: 2
#2Georgina Askeland (Oslo University Hospital)
Last. Zdenka EllederovaH-Index: 7
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Background Huntington´s disease (HD) is devastating neurodegenerative disorder caused by the mutation in huntingtin gene. One of the largest contributors to HD pathology represents oxidative stress, though the exact mechanism of its cause remains unclear. Molecular characterization of a unique porcine model of HD could serve for better understanding of the disease pathogenesis as well as for better evaluation of the therapeutic efficiency of preclinical studies on this large animal model. Aims I...
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#1Marie Rodinova (First Faculty of Medicine, Charles University in Prague)H-Index: 2
#2Jana Krizova (First Faculty of Medicine, Charles University in Prague)H-Index: 1
Last. Hana Hansikova (First Faculty of Medicine, Charles University in Prague)H-Index: 14
view all 12 authors...
Background Skeletal muscle wasting and atrophy is one of the severe clinical impairment connected with progression of Huntington’s disease (HD). Mitochondrial dysfunction may play significant role in aetiology of the HD but exact condition of mitochondria as the major energy-producing organelles during development of the HD in muscle has not yet been carefully investigated. The aim of the study was the longitudinal monitoring of mitochondrial function in skeletal muscle of transgenic minipigs ex...
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#1Georgina Askeland (University of Oslo)H-Index: 2
#2Zaneta Dosoudilova (Charles University in Prague)H-Index: 2
Last. Lars Eide (University of Oslo)H-Index: 20
view all 11 authors...
Huntington’s disease (HD) is a progressive neurodegenerative disorder primarily affecting the basal ganglia and is caused by expanded CAG repeats in the huntingtin gene. Except for CAG sizing, mitochondrial and nuclear DNA (mtDNA and nDNA) parameters have not yet proven to be representative biomarkers for disease and future therapy. Here, we identified a general suppression of genes associated with aerobic metabolism in peripheral blood mononuclear cells (PBMCs) from HD patients compared to cont...
5 CitationsSource
#1Katja Scheffler (Oslo University Hospital)H-Index: 10
#2Lyudmila I. Rachek (USA: University of South Alabama)H-Index: 16
Last. Lars Eide (Oslo University Hospital)H-Index: 20
view all 9 authors...
Abstract Mitochondrial DNA (mtDNA) resides in close proximity to metabolic reactions, and is maintained by the 8-oxoguanine DNA glycosylase (Ogg1) and other members of the base excision repair pathway. Here, we tested the hypothesis that changes in liver metabolism as under fasting/feeding conditions would be sensed by liver mtDNA, and that Ogg1 deficient mice might unravel a metabolic phenotype. Wild type (WT) and ogg1 −/− mice were either fed ad libitum or subjected to fasting for 24 h, and th...
3 CitationsSource
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