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dc.contributor.authorOma, Ingvild
dc.contributor.authorOlstad, Ole Kristoffer
dc.contributor.authorAndersen, Jacqueline Kirsti
dc.contributor.authorLyberg, Torstein
dc.contributor.authorMolberg, Øyvind
dc.contributor.authorFostad, Ida
dc.contributor.authorFagerland, Morten
dc.contributor.authorAlmdahl, Sven Martin
dc.contributor.authorRynning, Stein Erik
dc.contributor.authorYndestad, Arne
dc.contributor.authorAukrust, Pål
dc.contributor.authorWhist, Jon Elling
dc.contributor.authorHollan, Ivana
dc.coverage.spatialNorwaynb_NO
dc.date.accessioned2018-11-21T10:06:47Z
dc.date.available2018-11-21T10:06:47Z
dc.date.created2018-10-10T17:04:45Z
dc.date.issued2018
dc.identifier.citationPLoS ONE. 2018, 13:e0202346 (8), 1-13.nb_NO
dc.identifier.issn1932-6203
dc.identifier.urihttp://hdl.handle.net/11250/2574076
dc.description.abstractBACKGROUND: Vitamin D has an important role in the immune system, and has been linked to rheumatoid arthritis (RA) and coronary artery disease (CAD). The exact mechanisms by which vitamin D is involved in these processes are still unclear. Therefore, we wanted to search for differences in expression of genes involved in the vitamin D receptor (VDR) activation pathway and genes that are known to alter upon vitamin D stimulation, in the aortic adventitia of CAD patients with and without RA. METHODS: Affymetrix microarray was used to determine gene expression profile in surgical specimens from the adventitia of the ascending aorta of CAD patients with RA (n = 8) and without RA (n = 8) from the Feiring Heart Biopsy Study. RESULTS: We identified three vitamin D associated genes that were differentially expressed between RA and non-RA patients: Growth arrest and DNA-damage-inducible protein 45 alpha (GADD45A) (FC = 1.47; p = 0.006), Nuclear Receptor Co-repressor 1 (NCOR1) (FC = 1,21; p = 0.005) and paraoxonases 2 (PON2) (FC = -1.37; p = 0.01). High expression of GADD45A in RA tissues was confirmed by real-time qRT-PCR. GADD45A expression correlated with plasma levels of 1,25(OH)2D3 (rs = 0.69; p = 0.003). CONCLUSIONS: Microarray analyses revealed higher expression of GADD45A and NCOR1; and lower expression of PON2 in the aortic adventitia of RA than non-RA patients. Further studies are needed to elucidate if and how GADD45A, NCOR1 and PON2 are involved in the development of accelerated atherosclerosis in RA. In theory, some of these factors might have proatherogenic effects whereas others might reflect an underlying vascular pathology promoting atherogenesis (such as vascular stress).nb_NO
dc.description.sponsorshipThis study was supported by the Innlandet Hospital Trust, South-Eastern Norway Regional Health Authority, the Norwegian Women’s Public Health Association, the Norwegian Rheumatism Association, and the Norwegian Association for People with Heart and Lung Diseases.nb_NO
dc.language.isoengnb_NO
dc.relation.urihttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0202346
dc.rightsNavngivelse-Ikkekommersiell-DelPåSammeVilkår 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/deed.no*
dc.subjectVitamin Dnb_NO
dc.subjectimmune systemnb_NO
dc.subjectrheumatoid arthritisnb_NO
dc.subjectcoronary artery diseasenb_NO
dc.subjectascending aortanb_NO
dc.subjectDNAnb_NO
dc.subjectatherosclerosisnb_NO
dc.subjectvascular pathologynb_NO
dc.titleDifferential expression of Vitamin D associated genes in the aorta of coronary artery disease patients with and without rheumatoid arthritisnb_NO
dc.title.alternativeDifferential expression of Vitamin D associated genes in the aorta of coronary artery disease patients with and without rheumatoid arthritisnb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.description.versionpublishedVersionnb_NO
dc.rights.holder© 2018 Oma et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.nb_NO
dc.source.pagenumber1-13nb_NO
dc.source.volume13:e0202346nb_NO
dc.source.journalPLoS ONEnb_NO
dc.source.issue8nb_NO
dc.identifier.doi10.1371/journal.pone.0202346
dc.identifier.cristin1619467
cristin.unitcode1991,0,0,0
cristin.unitcode1991,7,0,0
cristin.unitcode1991,6,0,0
cristin.unitnameSykehuset Innlandet HF
cristin.unitnameDiv Medisinsk service
cristin.unitnameDiv Lillehammer
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1


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