Evidence map›Paper›PMID 30664710›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2019

OxHDL controls LOX-1 expression and plasma membrane localization through a mechanism dependent on NOX/ROS/NF-κB pathway on endothelial cells.

Lorena Pérez, Alejandro Vallejos, Cesar Echeverria, Diego Varela, Claudio Cabello-Verrugio, Felipe Simon

Erratum issuedOpen access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 47 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Lorena PérezDepartamento de Ciencias Biologicas, Facultad de Ciencias de la Vida, Universidad Andres Bello, Ave. Republica 239, 8370134, Santiago, Chile.
Alejandro VallejosDepartamento de Ciencias Biologicas, Facultad de Ciencias de la Vida, Universidad Andres Bello, Ave. Republica 239, 8370134, Santiago, Chile.
Cesar EcheverriaFacultad de Medicina, Universidad de Atacama, Copayapu 485, 1531772, Copiapo, Chile.
Diego VarelaPrograma de Fisiología y Biofísica, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, 8380453, Santiago, Chile.
Claudio Cabello-VerrugioDepartamento de Ciencias Biologicas, Facultad de Ciencias de la Vida, Universidad Andres Bello, Ave. Republica 239, 8370134, Santiago, Chile.
Felipe SimonDepartamento de Ciencias Biologicas, Facultad de Ciencias de la Vida, Universidad Andres Bello, Ave. Republica 239, 8370134, Santiago, Chile. fsimon@unab.cl.
Universidad Andrés Bello · CLMillennium Nucleus of Ion Channel Associated Diseases · CLUniversity of Atacama · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic inflammatory diseases enhance circulating oxidative stress levels, which results in the oxidation of circulating high-density lipoprotein (oxHDL). Endothelial cell function can be negatively impacted by oxHDL, but the underlying mechanisms for this remain unclear. Some reports indicate that the lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is also a receptor for oxHDL. However, it is unknown if oxHDL induces increased LOX-1 expression at the plasma membrane, as an event that supports endothelial dysfunction. Therefore, the aims of this study were to determine if oxHDL induces plasma-membrane level changes in LOX-1 and, if so, to describe the underlying mechanisms in endothelial cells. Our results demonstrate that the incubation of arterial or vein endothelial cells with oxHDL (and not HDL) induces the increase of LOX-1 expression at the plasma membrane; effect prevented by LOX-1 inhibition. Importantly, same results were observed in endothelial cells from oxHDL-treated rats. Furthermore, the observed oxHDL-induced LOX-1 expression is abolished by the down-regulation of NOX-2 expression with siRNA (and no others NOX isoforms), by the pharmacological inhibition of NAD(P)H oxidase (with DPI or apocynin) or by the inhibition of NF-κB transcription factor. Coherently, LOX-1 expression is augmented by the incubation of endothelial cells with H

Indexed as

AnimalsCell MembraneCells, CulturedEndothelial CellsHumansHuman Umbilical Vein Endothelial CellsInflammationLipoproteins, HDLMaleNADPH Oxidase 2NF-kappa BOxidation-ReductionOxidative StressRatsRats, Sprague-DawleyReactive Oxygen SpeciesLipoproteins, HDLNADPH Oxidase 2NF-kappa BOLR1 protein, humanOLR1 protein, ratReactive Oxygen SpeciesScavenger Receptors, Class E

Identifiers

PMID30664710
OpenAlexW2910414085

What OpenQuestion holds

Textmetadata
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.