dc.date.accessioned | 2021-12-22T16:15:21Z | |
dc.date.available | 2021-12-22T16:15:21Z | |
dc.date.created | 2021-07-09T14:54:55Z | |
dc.date.issued | 2021 | |
dc.identifier.citation | Wik, Jonas Aakre Phung, Danh Kolan, Shrikant Haraldsen, Guttorm Skålhegg, Bjørn Steen Hol Fosse, Johanna . Inflammatory activation of endothelial cells increases glycolysis and oxygen consumption despite inhibiting cell proliferation. FEBS Open Bio. 2021, 11(6), 1719-1730 | |
dc.identifier.uri | http://hdl.handle.net/10852/89784 | |
dc.description.abstract | Endothelial cell function and metabolism are closely linked to differential use of energy substrate sources and combustion. While endothelial cell migration is promoted by 2-phosphofructokinase-6/fructose-2,6-bisphosphatase (PFKFB3)-driven glycolysis, proliferation also depends on fatty acid oxidation for dNTP synthesis. We show that inflammatory activation of human umbilical vein endothelial cells (HUVECs) by interleukin-1β (IL-1β), despite inhibiting proliferation, promotes a shift toward more metabolically active phenotype. This was reflected in increased cellular glucose uptake and consumption, which was preceded by an increase in PFKFB3 mRNA and protein expression. However, despite a modest increase in extracellular acidification rates, the increase in glycolysis did not correlate with extracellular lactate accumulation. Accordingly, IL-1β stimulation also increased oxygen consumption rate, but without a concomitant rise in fatty acid oxidation. Together, this suggests that the IL-1β-stimulated energy shift is driven by shunting of glucose-derived pyruvate into mitochondria to maintain elevated oxygen consumption in HUVECs. We also revealed a marked donor-dependent variation in the amplitude of the metabolic response to IL-1β and postulate that the donor-specific response should be taken into account when considering targeting dysregulated endothelial cell metabolism. | |
dc.language | EN | |
dc.rights | Attribution 4.0 International | |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0/ | |
dc.title | Inflammatory activation of endothelial cells increases glycolysis and oxygen consumption despite inhibiting cell proliferation | |
dc.type | Journal article | |
dc.creator.author | Wik, Jonas Aakre | |
dc.creator.author | Phung, Danh | |
dc.creator.author | Kolan, Shrikant | |
dc.creator.author | Haraldsen, Guttorm | |
dc.creator.author | Skålhegg, Bjørn Steen | |
dc.creator.author | Hol Fosse, Johanna | |
cristin.unitcode | 185,53,18,13 | |
cristin.unitname | Avdeling for patologi | |
cristin.ispublished | true | |
cristin.fulltext | original | |
cristin.qualitycode | 1 | |
dc.identifier.cristin | 1921216 | |
dc.identifier.bibliographiccitation | info:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=FEBS Open Bio&rft.volume=11&rft.spage=1719&rft.date=2021 | |
dc.identifier.jtitle | FEBS Open Bio | |
dc.identifier.volume | 11 | |
dc.identifier.issue | 6 | |
dc.identifier.startpage | 1719 | |
dc.identifier.endpage | 1730 | |
dc.identifier.doi | https://doi.org/10.1002/2211-5463.13174 | |
dc.identifier.urn | URN:NBN:no-92384 | |
dc.type.document | Tidsskriftartikkel | |
dc.type.peerreviewed | Peer reviewed | |
dc.source.issn | 2211-5463 | |
dc.identifier.fulltext | Fulltext https://www.duo.uio.no/bitstream/handle/10852/89784/2/2211-5463.13174.pdf | |
dc.type.version | PublishedVersion | |