Evidence map›Paper›PMID 33979025›Full record

ArticleFEBS open bio2021

Inflammatory activation of endothelial cells increases glycolysis and oxygen consumption despite inhibiting cell proliferation.

Jonas Aakre Wik, Danh Phung, Shrikant Kolan, Guttorm Haraldsen, Bjørn Steen Skålhegg, Johanna Hol Fosse

Open access · goldAbstract read
In one paragraph

Article in FEBS open bio, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 35% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 21 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Jonas Aakre WikDepartment of Pathology, Oslo University Hospital-Rikshospitalet, Norway.ORCID 0000-0003-3065-5529
Danh PhungDepartment of Pathology, Oslo University Hospital-Rikshospitalet, Norway.
Shrikant KolanDepartment of Nutrition, Division of Molecular Nutrition, Institute of Basic Medical Sciences, University of Oslo, Norway.ORCID 0000-0002-0683-6226
Guttorm HaraldsenDepartment of Pathology, Oslo University Hospital-Rikshospitalet, Norway.
Bjørn Steen SkålheggDepartment of Nutrition, Division of Molecular Nutrition, Institute of Basic Medical Sciences, University of Oslo, Norway.
Johanna Hol FosseDepartment of Pathology, Oslo University Hospital-Rikshospitalet, Norway.ORCID 0000-0001-5837-5006
Oslo University Hospital · NOUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

ApoptosisCell ProliferationCells, CulturedGlycolysisHumansHuman Umbilical Vein Endothelial CellsInflammationInterleukin-1betaOxygen ConsumptionIL1B protein, humanInterleukin-1betaendothelial cellsglycolysisIL-1βinflammationmetabolism

Identifiers

PMID33979025
PMCPMC8167874
OpenAlexW3162223320

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.