Evidence map›Paper›PMID 31823799›Full record

ArticleLipids in health and disease2019

CPT1a gene expression reverses the inflammatory and anti-phagocytic effect of 7-ketocholesterol in RAW264.7 macrophages.

Priscila Calle, Angeles Muñoz, Anna Sola, Georgina Hotter

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

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  16. Development of Cell Therapies for Renal Disease and Regenerative Medicine.International journal of molecular sciences · 2022
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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

4 authors at 2 institutions in 1 country.

Priscila CalleDepartment of Experimental Pathology, Institut d'Investigacions Biomèdiques de Barcelona-Consejo Superior de Investigaciones Científicas-Institut d'Investigacions Biomèdiques August Pi i Sunyer (IIBB-CSIC-IDIBAPS), Rosselló 161, 7th floor, 08036, Barcelona, Spain.
Angeles MuñozDepartment of Experimental Pathology, Institut d'Investigacions Biomèdiques de Barcelona-Consejo Superior de Investigaciones Científicas-Institut d'Investigacions Biomèdiques August Pi i Sunyer (IIBB-CSIC-IDIBAPS), Rosselló 161, 7th floor, 08036, Barcelona, Spain.
Anna SolaDepartment of Experimental Nephrology, Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), Hospitalet de Llobregat, Barcelona, Spain.
Georgina HotterDepartment of Experimental Pathology, Institut d'Investigacions Biomèdiques de Barcelona-Consejo Superior de Investigaciones Científicas-Institut d'Investigacions Biomèdiques August Pi i Sunyer (IIBB-CSIC-IDIBAPS), Rosselló 161, 7th floor, 08036, Barcelona, Spain. georgina.hotter@iibb.csic.es.ORCID http://orcid.org/0000-0001-7324-1305
Consejo Superior de Investigaciones Científicas · ESInstitut d'Investigació Biomédica de Bellvitge · ES

Funding

Fondo de Investigación sanitaria PI17/01411Ministerio de Economía y Competitividad SAF2015-67770-R
6 · The paper itself

Abstract

backgroundMacrophage are specialized cells that contributes to the removal of detrimental contents via phagocytosis. Lipid accumulation in macrophages, whether from phagocytosis of dying cells or from circulating oxidized low-density lipoproteins, alters macrophage biology and functionality. It is known that carnitine palmitoyl transferase 1-a (CPT1a) gene encodes an enzyme involved in fatty acid oxidation and, therefore, lipid content. However, the potential of CPT1a to activate macrophage phagocytic function have not been elucidated.

methodsUsing a murine macrophage cell line, RAW264.7, we determine if intracellular accumulation of 7-ketocholesterol (7-KC) modulates macrophage phagocytic function through CPT1a gene expression. In addition, the effects of CPT1a genetic modification on macrophage phenotype and phagocytosis has been studied.

resultsOur results revealed that CPT1a gene expression decreased by the accumulation of 7-KC at the higher dose of 7-KC. This was concomitant with an impair ability to phagocytize bioparticles and an inflammatory phenotype. GW3965 treatment, which have shown to facilitate the efflux of cholesterol, eliminated the intracellular lipid droplets of 7-KC-laden macrophages, increased the gene expression of CPT1a, diminished the gene expression of the inflammatory marker iNOS and restored macrophage phagocytosis. Furthermore, CPT1a Knockdown per se was detrimental for macrophage phagocytosis whereas transcriptional activation of CPT1a heightened the uptake of bioparticles.

conclusionsAltogether, our findings indicate that downregulation of CPT1a by lipid content modulates macrophage phagocytosis and inflammatory phenotype.

Indexed as

InflammationAnimalsCarnitine O-PalmitoyltransferaseDown-RegulationGene ExpressionGene Knockdown TechniquesKetocholesterolsMacrophage ActivationMacrophagesMicePhagocytosisRAW 264.7 CellsTransfection7-ketocholesterolCarnitine O-PalmitoyltransferaseCPT1B protein, mouseKetocholesterols7-ketocholesterolCPT1aInflammationMacrophagePhagocytosis

Identifiers

PMID31823799
PMCPMC6902499
OpenAlexW2996527230

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Registered trials

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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.