Evidence map›Paper›PMID 26463174›Full record

ArticleJournal of translational medicine2015

Monocytes/macrophages activation contributes to b-gamma-glutamyltransferase accumulation inside atherosclerotic plaques.

Eugenia Belcastro, Maria Franzini, Silvana Cianchetti, Evelina Lorenzini, Silvia Masotti, Vanna Fierabracci, Angela Pucci, Alfonso Pompella, Alessandro Corti

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 26% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
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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

9 authors at 2 institutions in 2 countries.

Eugenia BelcastroDepartment of Translational Research and New Technologies in Medicine and Surgery, Medical School, University of Pisa, Via Roma 55, 56126, Pisa, Italy. eugenia.belcastro@virgilio.it.
Maria FranziniDepartment of Translational Research and New Technologies in Medicine and Surgery, Medical School, University of Pisa, Via Roma 55, 56126, Pisa, Italy. maria.franzini@unipi.it.
Silvana CianchettiDepartment of Surgery and Medical, Molecular, and Critical Area Pathology, Medical School, University of Pisa, Pisa, Italy. silvana.cianchetti@dctv.unipi.it.
Evelina LorenziniDepartment of Translational Research and New Technologies in Medicine and Surgery, Medical School, University of Pisa, Via Roma 55, 56126, Pisa, Italy. evelina.lorenzini@dps.unipi.it.
Silvia MasottiLife Science Institute, Scuola Superiore Sant'Anna, Pisa, Italy. silvi87@gmail.com.
Vanna FierabracciDepartment of Translational Research and New Technologies in Medicine and Surgery, Medical School, University of Pisa, Via Roma 55, 56126, Pisa, Italy. vanna.fierabracci@med.unipi.it.
Angela PucciHistopathology Department, University Hospital, Pisa, Italy. a.pucci@ao-pisa.toscana.it.
Alfonso PompellaDepartment of Translational Research and New Technologies in Medicine and Surgery, Medical School, University of Pisa, Via Roma 55, 56126, Pisa, Italy. alfonso.pompella@med.unipi.it.
Alessandro CortiDepartment of Translational Research and New Technologies in Medicine and Surgery, Medical School, University of Pisa, Via Roma 55, 56126, Pisa, Italy. alessandro.corti@med.unipi.it.
University of Pisa · ITScuola Superiore Sant'Anna · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGamma-glutamyltransferase (GGT) is a well-established independent risk factor for cardiovascular mortality related to atherosclerotic disease. Four GGT fractions have been identified in plasma, but only b-GGT fraction accumulates in atherosclerotic plaques, and correlates with other histological markers of vulnerability. The present study was aimed to evaluate whether macrophagic lineage cells may provide a source of b-GGT within the atherosclerotic plaque.

methodsGGT expression and release were studied in human monocytes isolated from peripheral blood of healthy donors. The growth factors GM-CSF and M-CSF were used to induce differentiation into M1-like and M2-like macrophages, respectively. Plaque GGT was investigated in tissue samples obtained from patients undergoing carotid endoarterectomy.

resultsWe found that M1-like macrophages express higher levels of GGT as compared to M2-like, and that both monocytes and M1-like macrophages-but not M2-like-are able to release the b-GGT fraction upon activation with pro-inflammatory stimuli. Western blot analysis of b-GGT extracted from plaques confirmed the presence of a GGT immunoreactive peptide coincident with that of macrophages.

conclusionsOur data indicate that macrophages characterized by a pro-inflammatory phenotype may contribute to intra-plaque accumulation of b-GGT, which in turn may play a role in the progression of atherosclerosis by modulating inflammatory processes and favouring plaque instability.

Indexed as

Gene Expression RegulationCell DifferentiationCell LineageChromatography, GelDisease ProgressionEndarterectomy, Carotidgamma-GlutamyltransferaseGranulocyte-Macrophage Colony-Stimulating FactorHealthy VolunteersHumansInflammationLeukocytes, MononuclearMacrophage Colony-Stimulating FactorMacrophagesMicrocirculationMonocytesgamma-GlutamyltransferaseGranulocyte-Macrophage Colony-Stimulating FactorMacrophage Colony-Stimulating Factor

Identifiers

PMID26463174
PMCPMC4604102
OpenAlexW1946189800

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LicenceCC BY
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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.