Hide metadata

dc.date.accessioned2020-05-09T19:37:25Z
dc.date.available2020-05-09T19:37:25Z
dc.date.created2019-12-05T09:40:36Z
dc.date.issued2020
dc.identifier.citationNarverud, Ingunn Christensen, Jacob J. Bakke, Siril Skaret Ulven, Stine Marie Rundblad, Amanda Aukrust, Pål Espevik, Terje Bogsrud, Martin Prøven Retterstøl, Kjetil Ueland, Thor Halvorsen, Bente Holven, Kirsten Bjørklund . Profiling of immune-related gene expression in children with familial hypercholesterolaemia. Journal of Internal Medicine. 2019, 1-12
dc.identifier.urihttp://hdl.handle.net/10852/75336
dc.description.abstractBackground Innate and adaptive immune responses are pivotal in atherosclerosis, but their association with early‐stage atherosclerosis in humans is incompletely understood. In this regard, untreated children with familial hypercholesterolaemia may serve as a human model to investigate the effect of elevated low‐density lipoprotein (LDL)‐cholesterol. Objectives We aimed to study the immunological and inflammatory pathways involved in early atherosclerosis by examining mRNA molecules in peripheral blood mononuclear cells (PBMCs) from children with FH. Methods We analysed the level of 587 immune‐related mRNA molecules using state‐of‐the‐art Nanostring technology in PBMCs from children with (n = 30) and without (n = 21) FH, and from FH children before and after statin therapy (n = 10). Results 176 genes (30%) were differentially expressed between the FH and healthy children at P < 0.05. Compared to healthy children, the dysregulated pathways in FH children included the following: T cells (18/19); B cells (5/6); tumour necrosis factor super family (TNFSF) (6/8); cell growth, proliferation and differentiation (5/7); interleukins (5/9); toll‐like receptors (2/5); apoptosis (3/7) and antigen presentation (1/7), where the ratio denotes higher expressed genes to total number of genes. Statin therapy reversed expression of thirteen of these mRNAs in FH children. Conclusion FH children display higher PBMC expression of immune‐related genes mapped to several pathways, including T and B cells, and TNFSF than healthy children. Our results suggest that LDL‐C plays an important role in modulating expression of different immune‐related genes, and novel data on the involvement of these pathways in the early atherosclerosis may represent future therapeutic targets for prevention of atherosclerotic progression.
dc.languageEN
dc.publisherBlackwell Science Ltd.
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.titleProfiling of immune-related gene expression in children with familial hypercholesterolaemia
dc.typeJournal article
dc.creator.authorNarverud, Ingunn
dc.creator.authorChristensen, Jacob J.
dc.creator.authorBakke, Siril Skaret
dc.creator.authorUlven, Stine Marie
dc.creator.authorRundblad, Amanda
dc.creator.authorAukrust, Pål
dc.creator.authorEspevik, Terje
dc.creator.authorBogsrud, Martin Prøven
dc.creator.authorRetterstøl, Kjetil
dc.creator.authorUeland, Thor
dc.creator.authorHalvorsen, Bente
dc.creator.authorHolven, Kirsten Bjørklund
cristin.unitcode185,51,13,22
cristin.unitnameKosthold og aterosklerose
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1
dc.identifier.cristin1756956
dc.identifier.bibliographiccitationinfo:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Journal of Internal Medicine&rft.volume=&rft.spage=1&rft.date=2019
dc.identifier.jtitleJournal of Internal Medicine
dc.identifier.volume287
dc.identifier.issue3
dc.identifier.startpage310
dc.identifier.endpage321
dc.identifier.doihttps://doi.org/10.1111/joim.13001
dc.identifier.urnURN:NBN:no-78405
dc.type.documentTidsskriftartikkel
dc.type.peerreviewedPeer reviewed
dc.source.issn0954-6820
dc.identifier.fulltextFulltext https://www.duo.uio.no/bitstream/handle/10852/75336/2/Profiling%2Bof%2Bimmune-related%2Bgene%2Bexpression%2Bin%2Bchildren%2Bwithfamilial%2Bhypercholesterolaemia.pdf
dc.type.versionPublishedVersion
dc.relation.projectNFR/223255


Files in this item

Appears in the following Collection

Hide metadata

Attribution 4.0 International
This item's license is: Attribution 4.0 International