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dc.date.accessioned2018-08-17T07:37:53Z
dc.date.available2018-08-17T07:37:53Z
dc.date.created2018-07-03T12:49:02Z
dc.date.issued2018
dc.identifier.citationBrinchmann, Bendik Christian Le Ferrec, Eric Podechard, Normand Lagadic-Gossmann, Dominique Shoji, Kenji F. Penna, Aubin Kukowski, Klara Kubátová, Alena Holme, Jørn Andreas Øvrevik, Johan . Lipophilic chemicals from diesel exhaust particles trigger calcium response in human endothelial cells via aryl hydrocarbon receptor non-genomic signalling. International Journal of Molecular Sciences. 2018, 19(5)
dc.identifier.urihttp://hdl.handle.net/10852/63026
dc.description.abstractExposure to diesel exhaust particles (DEPs) affects endothelial function and may contribute to the development of atherosclerosis and vasomotor dysfunction. As intracellular calcium concentration [Ca2+]i is considered important in myoendothelial signalling, we explored the effects of extractable organic matter from DEPs (DEP-EOM) on [Ca2+]i and membrane microstructure in endothelial cells. DEP-EOM of increasing polarity was obtained by pressurized sequential extraction of DEPs with n-hexane (n-Hex-EOM), dichloromethane (DCM-EOM), methanol, and water. Chemical analysis revealed that the majority of organic matter was extracted by the n-Hex- and DCM-EOM, with polycyclic aromatic hydrocarbons primarily occurring in n-Hex-EOM. The concentration of calcium was measured in human microvascular endothelial cells (HMEC-1) using micro-spectrofluorometry. The lipophilic n-Hex-EOM and DCM-EOM, but not the more polar methanol- and water-soluble extracts, induced rapid [Ca2+]i increases in HMEC-1. n-Hex-EOM triggered [Ca2+]i increase from intracellular stores, followed by extracellular calcium influx consistent with store operated calcium entry (SOCE). By contrast, the less lipophilic DCM-EOM triggered [Ca2+]i increase via extracellular influx alone, resembling receptor operated calcium entry (ROCE). Both extracts increased [Ca2+]i via aryl hydrocarbon receptor (AhR) non-genomic signalling, verified by pharmacological inhibition and RNA-interference. Moreover, DCM-EOM appeared to induce an AhR-dependent reduction in the global plasma membrane order, as visualized by confocal fluorescence microscopy. DCM-EOM-triggered [Ca2+]i increase and membrane alterations were attenuated by the membrane stabilizing lipid cholesterol. In conclusion, lipophilic constituents of DEPs extracted by n-hexane and DCM seem to induce rapid AhR-dependent [Ca2+]i increase in HMEC-1 endothelial cells, possibly involving both ROCE and SOCE-mediated mechanisms. The semi-lipophilic fraction extracted by DCM also caused an AhR-dependent reduction in global membrane order, which appeared to be connected to the [Ca2+]i increase.en_US
dc.languageEN
dc.language.isoenen_US
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.titleLipophilic chemicals from diesel exhaust particles trigger calcium response in human endothelial cells via aryl hydrocarbon receptor non-genomic signallingen_US
dc.title.alternativeENEngelskEnglishLipophilic chemicals from diesel exhaust particles trigger calcium response in human endothelial cells via aryl hydrocarbon receptor non-genomic signalling
dc.typeJournal articleen_US
dc.creator.authorBrinchmann, Bendik Christian
dc.creator.authorLe Ferrec, Eric
dc.creator.authorPodechard, Normand
dc.creator.authorLagadic-Gossmann, Dominique
dc.creator.authorShoji, Kenji F.
dc.creator.authorPenna, Aubin
dc.creator.authorKukowski, Klara
dc.creator.authorKubátová, Alena
dc.creator.authorHolme, Jørn Andreas
dc.creator.authorØvrevik, Johan
cristin.unitcode185,53,18,13
cristin.unitnameAvdeling for patologi
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1
dc.identifier.cristin1595415
dc.identifier.bibliographiccitationinfo:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=International Journal of Molecular Sciences&rft.volume=19&rft.spage=&rft.date=2018
dc.identifier.jtitleInternational Journal of Molecular Sciences
dc.identifier.volume19
dc.identifier.issue5
dc.identifier.pagecount20
dc.identifier.doihttp://dx.doi.org/10.3390/ijms19051429
dc.identifier.urnURN:NBN:no-65590
dc.type.documentTidsskriftartikkelen_US
dc.type.peerreviewedPeer reviewed
dc.source.issn1422-0067
dc.identifier.fulltextFulltext https://www.duo.uio.no/bitstream/handle/10852/63026/2/Brinchmann_Int%2BJ%2BMol%2BSci_post%2B1595415.pdf
dc.type.versionPublishedVersion
cristin.articleid1429


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