Evidence map›Paper›PMID 30658193›Full record

ArticleAtherosclerosis2019

GPVI surface expression and signalling pathway activation are increased in platelets from obese patients: Elucidating potential anti-atherothrombotic targets in obesity.

María N Barrachina, Aurelio M Sueiro, Irene Izquierdo, Lidia Hermida-Nogueira, Esteban Guitián, Felipe F Casanueva, Richard W Farndale, Masaaki Moroi, Stephanie M Jung, María Pardo and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Atherosclerosis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

35 citing papers in PubMed, 49 citations in OpenAlex.

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  9. Western Diet Modifies Platelet Activation Profiles in Male Mice.International journal of molecular sciences · 2024
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  13. Heterogeneity of platelets and their responses.Research and practice in thrombosis and haemostasis · 2024
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  17. DIGE Analysis of Clinical Specimens.Methods in molecular biology (Clifton, N.J.) · 2023
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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

11 authors at 4 institutions in 2 countries.

María N BarrachinaPlatelet Proteomics Group, Center for Research in Molecular Medicine and Chronic Diseases (CIMUS), Universidade Santiago de Compostela, Santiago de Compostela, Spain; Instituto de Investigación Sanitaria de Santiago (IDIS), Santiago de Compostela, Spain.
Aurelio M SueiroGrupo de Endocrinología Molecular y Celular - Instituto de Investigación Sanitaria de Santiago (IDIS)/ Servicio de Endocrinología, Xerencia de Xestión Integrada de Santiago (XXS), Santiago de Compostela, Spain.
Irene IzquierdoPlatelet Proteomics Group, Center for Research in Molecular Medicine and Chronic Diseases (CIMUS), Universidade Santiago de Compostela, Santiago de Compostela, Spain; Instituto de Investigación Sanitaria de Santiago (IDIS), Santiago de Compostela, Spain.
Lidia Hermida-NogueiraPlatelet Proteomics Group, Center for Research in Molecular Medicine and Chronic Diseases (CIMUS), Universidade Santiago de Compostela, Santiago de Compostela, Spain; Instituto de Investigación Sanitaria de Santiago (IDIS), Santiago de Compostela, Spain.
Esteban GuitiánMass Spectrometry and Proteomic Unit, Rede de Infraestructuras de Apoio á Investigación e ao Desenvolvemento Tecnolóxico, Universidade de Santiago de Compostela, Santiago de Compostela, Spain.
Felipe F CasanuevaInstituto de Investigación Sanitaria de Santiago (IDIS), Santiago de Compostela, Spain; Grupo de Endocrinología Molecular y Celular - Instituto de Investigación Sanitaria de Santiago (IDIS)/ Servicio de Endocrinología, Xerencia de Xestión Integrada de Santiago (XXS), Santiago de Compostela, Spain.
Richard W FarndaleDepartment of Biochemistry, University of Cambridge, Cambridge, CB2 1QW, United Kingdom.
Masaaki MoroiDepartment of Biochemistry, University of Cambridge, Cambridge, CB2 1QW, United Kingdom.
Stephanie M JungDepartment of Biochemistry, University of Cambridge, Cambridge, CB2 1QW, United Kingdom.
María PardoInstituto de Investigación Sanitaria de Santiago (IDIS), Santiago de Compostela, Spain; Grupo Obesidómica - Instituto de Investigación Sanitaria de Santiago (IDIS), Santiago de Compostela, Spain.
Ángel GarcíaPlatelet Proteomics Group, Center for Research in Molecular Medicine and Chronic Diseases (CIMUS), Universidade Santiago de Compostela, Santiago de Compostela, Spain; Instituto de Investigación Sanitaria de Santiago (IDIS), Santiago de Compostela, Spain. Electronic address: angel.garcia@usc.es.
Center for Research in Molecular Medicine and Chronic Diseases · ESInstituto de Investigación Sanitaria de Santiago · ESUniversity of Cambridge · GBUniversidade de Santiago de Compostela · ES

Funding

British Heart Foundation PG/10/011/28199British Heart Foundation PG/18/36/33811British Heart Foundation RG/15/4/31268British Heart Foundation SP/13/7/30575
6 · The paper itself

Abstract

BACKGROUND AND

aimsPlatelets play a fundamental role in the increased atherothrombotic risk related to central obesity since they show hyperactivation and lower sensitivity to antiplatelet therapy in obese patients. The main goal of this study was to identify platelet biomarkers related to the risk of atherothrombosis in obese patients, confirm platelet activation levels in these patients, and identify altered activation pathways.

methodsPlatelets were obtained from cohorts of obese patients and age- and sex-matched lean controls. Biochemical and proteome analyses were done by two-dimensional differential in-gel electrophoresis (2D-DIGE), mass spectrometry, and immunoblotting. Functional and mechanistic studies were conducted with aggregation assays and flow cytometry.

resultsWe confirmed an up-regulation of αIIb and fibrinogen isoforms in platelets from obese patients. A complementary platelet aggregation approach showed platelets from obese patients are hyper-reactive in response to collagen and collagen-related peptide (CRP), revealing the collagen receptor Glycoprotein VI (GPVI) signalling as one of the altered pathways. We also found the active form of Src (pTyr418) is up-regulated in platelets from obese individuals, which links proteomics to aggregation data. Moreover, we showed that CRP-activated platelets present higher levels of tyrosine phosphorylated PLCγ2 in obese patients, confirming alterations in GPVI signalling. In line with the above, flow cytometry studies show higher surface expression levels of total GPVI and GPVI-dimer in obese platelets, both correlating with BMI.

conclusionsOur results suggest a higher activation state of SFKs-mediated signalling pathways in platelets from obese patients, with a primary involvement of GPVI signalling.

Indexed as

Platelet ActivationAdolescentAdultBlood PlateletsBody Mass IndexCase-Control StudiesFemaleHumansMaleObesityPhospholipase C gammaPhosphorylationPlatelet AggregationPlatelet Membrane GlycoproteinsSignal TransductionUp-RegulationPhospholipase C gammaPlatelet Membrane Glycoproteinsplatelet membrane glycoprotein VIDrug targetsGPVI signallingObesityPlateletsProteomicsSFK-Mediated signalling pathways

Identifiers

PMID30658193
PMCPMC6403451
OpenAlexW2906081335

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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.