Evidence map›Paper›PMID 26184769›Full record

ArticleFluids and barriers of the CNS2015

Cultured cells of the blood-brain barrier from apolipoprotein B-100 transgenic mice: effects of oxidized low-density lipoprotein treatment.

Nikolett Lénárt, Fruzsina R Walter, Alexandra Bocsik, Petra Sántha, Melinda E Tóth, András Harazin, Andrea E Tóth, Csaba Vizler, Zsolt Török, Ana-Maria Pilbat and 4 more

Open access · goldAbstract read
In one paragraph

Article in Fluids and barriers of the CNS, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 40 citations in OpenAlex.

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  10. Journal of immunology (Baltimore, Md. : 1950) · 2021
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  20. Activation of integrin α5 mediated by flow requires its translocation to membrane lipid rafts in vascular endothelial cells.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
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

14 authors at 5 institutions in 1 country.

Nikolett LénártLaboratory of Animal Genetics and Molecular Neurobiology, Institute of Biochemistry, Biological Research Centre, Hungarian Academy of Sciences, Temesvári krt. 62, 6720, Szeged, Hungary. lenart.nikolett@koki.mta.hu.
Fruzsina R WalterBiological Barriers Research Group, Institute of Biophysics, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary. walter.fruzsina@brc.mta.hu.
Alexandra BocsikBiological Barriers Research Group, Institute of Biophysics, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary. bocsik.alexandra@brc.mta.hu.
Petra SánthaBiological Barriers Research Group, Institute of Biophysics, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary. santha.petra@brc.mta.hu.
Melinda E TóthLaboratory of Animal Genetics and Molecular Neurobiology, Institute of Biochemistry, Biological Research Centre, Hungarian Academy of Sciences, Temesvári krt. 62, 6720, Szeged, Hungary. toth.erzsebet.melinda@brc.mta.hu.
András HarazinBiological Barriers Research Group, Institute of Biophysics, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary. harazin.andras@brc.mta.hu.
Andrea E TóthBiological Barriers Research Group, Institute of Biophysics, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary. toth.andrea.e@gmail.com.
Csaba VizlerLaboratory of Molecular Stress Biology, Institute of Biochemistry, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary. vizler.csaba@brc.mta.hu.
Zsolt TörökLaboratory of Molecular Stress Biology, Institute of Biochemistry, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary. torok.zsolt@brc.mta.hu.
Ana-Maria PilbatLaboratory of Molecular Stress Biology, Institute of Biochemistry, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary. pilbat.ana_maria@brc.mta.hu.
László VíghLaboratory of Molecular Stress Biology, Institute of Biochemistry, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary. vigh.laszlo@brc.mta.hu.
László G PuskásLaboratory of Functional Genomics, Laboratories of Core Facilities, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary. laszlo@avidinbiotech.com.
Miklós SánthaLaboratory of Animal Genetics and Molecular Neurobiology, Institute of Biochemistry, Biological Research Centre, Hungarian Academy of Sciences, Temesvári krt. 62, 6720, Szeged, Hungary. santha.miklos@brc.mta.hu.
Mária A DeliBiological Barriers Research Group, Institute of Biophysics, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary. deli.maria@brc.mta.hu.
Hungarian Academy of Sciences · HUHUN-REN Szegedi Biológiai Kutatóközpont · HUHUN-REN Institute of Experimental Medicine · HUInstitute of Biochemistry · HUInstitute of Biophysics · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe apolipoprotein B-100 (ApoB-100) transgenic mouse line is a model of human atherosclerosis. Latest findings suggest the importance of ApoB-100 in the development of neurodegenerative diseases and microvascular/perivascular localization of ApoB-100 protein was demonstrated in the cerebral cortex of ApoB-100 transgenic mice. The aim of the study was to characterize cultured brain endothelial cells, pericytes and glial cells from wild-type and ApoB-100 transgenic mice and to study the effect of oxidized low-density lipoprotein (oxLDL) on these cells.

methodsMorphology of cells isolated from brains of wild type and ApoB-100 transgenic mice was characterized by immunohistochemistry and the intensity of immunolabeling was quantified by image analysis. Toxicity of oxLDL treatment was monitored by real-time impedance measurement and lactate dehydrogenase release. Reactive oxygen species and nitric oxide production, barrier permeability in triple co-culture blood-brain barrier model and membrane fluidity were also determined after low-density lipoprotein (LDL) or oxLDL treatment.

resultsThe presence of ApoB-100 was confirmed in brain endothelial cells, while no morphological change was observed between wild type and transgenic cells. Oxidized but not native LDL exerted dose-dependent toxicity in all three cell types, induced barrier dysfunction and increased reactive oxygen species (ROS) production in both genotypes. A partial protection from oxLDL toxicity was seen in brain endothelial and glial cells from ApoB-100 transgenic mice. Increased membrane rigidity was measured in brain endothelial cells from ApoB-100 transgenic mice and in LDL or oxLDL treated wild type cells.

conclusionThe morphological and functional properties of cultured brain endothelial cells, pericytes and glial cells from ApoB-100 transgenic mice were characterized and compared to wild type cells for the first time. The membrane fluidity changes in ApoB-100 transgenic cells related to brain microvasculature indicate alterations in lipid composition which may be linked to the partial protection against oxLDL toxicity.

Indexed as

AnimalsApolipoprotein B-100AtherosclerosisBlood-Brain BarrierCells, CulturedCell SurvivalDisease Models, AnimalEndothelial CellsLipoproteins, LDLMembrane FluidityMiceMice, Inbred C57BLMice, TransgenicNeurogliaNitric OxidePericytesApolipoprotein B-100Lipoproteins, LDLNitric Oxideoxidized low density lipoproteinReactive Oxygen Species

Identifiers

PMID26184769
PMCPMC4504453
OpenAlexW1711797882

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.