Evidence map›Paper›PMID 35085240›Full record

ArticlePloS one2022

Impact of high platelet turnover on the platelet transcriptome: Results from platelet RNA-sequencing in patients with sepsis.

Thomas G Nührenberg, Jasmin Stöckle, Federico Marini, Mark Zurek, Björn A Grüning, Vladimir Benes, Lutz Hein, Franz-Josef Neumann, Christian Stratz, Marco Cederqvist and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Observational
  5. Alterations in RNA Expression Profile FollowingInternational journal of molecular sciences · 2025
    Article
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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 1 country.

Thomas G NührenbergKlinik für Kardiologie und Angiologie II, Universitätsklinik Freiburg, Universitäts-Herzzentrum Campus Bad Krozingen, Bad Krozingen, Germany.ORCID 0000-0001-7675-7120
Jasmin StöckleKlinik für Kardiologie und Angiologie II, Universitätsklinik Freiburg, Universitäts-Herzzentrum Campus Bad Krozingen, Bad Krozingen, Germany.
Federico MariniInstitut für Medizinische Biometrie, Epidemiologie und Informatik, Universitätsmedizin der Johannes-Gutenberg-Universität Mainz, Mainz, Germany.ORCID 0000-0003-3252-7758
Mark ZurekKlinik für Kardiologie und Angiologie II, Universitätsklinik Freiburg, Universitäts-Herzzentrum Campus Bad Krozingen, Bad Krozingen, Germany.
Björn A GrüningInstitut für Informatik, Albert-Ludwigs-Universität Freiburg, Freiburg, Germany.
Vladimir BenesGenomics Core Facility, European Molecular Biology Laboratory, Heidelberg, Germany.
Lutz HeinInstitut für experimentelle und klinische Pharmakologie und Toxikologie, Medizinische Fakultät, Albert-Ludwigs-Universität Freiburg, Freiburg, Germany.
Franz-Josef NeumannKlinik für Kardiologie und Angiologie II, Universitätsklinik Freiburg, Universitäts-Herzzentrum Campus Bad Krozingen, Bad Krozingen, Germany.ORCID 0000-0002-0921-8351
Christian StratzKlinik für Kardiologie und Angiologie II, Universitätsklinik Freiburg, Universitäts-Herzzentrum Campus Bad Krozingen, Bad Krozingen, Germany.
Marco CederqvistKlinik für Kardiologie und Angiologie II, Universitätsklinik Freiburg, Universitäts-Herzzentrum Campus Bad Krozingen, Bad Krozingen, Germany.
Willibald HochholzerKlinik für Kardiologie und Angiologie II, Universitätsklinik Freiburg, Universitäts-Herzzentrum Campus Bad Krozingen, Bad Krozingen, Germany.
Universitäts-Herzzentrum Freiburg-Bad Krozingen · DEUniversity of Freiburg · DEEuropean Molecular Biology Laboratory · DEJohannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSepsis is associated with high platelet turnover and elevated levels of immature platelets. Changes in the platelet transcriptome and the specific impact of immature platelets on the platelet transcriptome remain unclear. Thus, this study sought to address whether and how elevated levels of immature platelets affect the platelet transcriptome in patients with sepsis.

methodsBlood samples were obtained from patients with sepsis requiring vasopressor therapy (n = 8) and from a control group of patients with stable coronary artery disease and otherwise similar demographic characteristics (n = 8). Immature platelet fraction (IPF) was determined on a Sysmex XE 2100 analyser and platelet function was tested by impedance aggregometry. RNA from leukocyte-depleted platelets was used for transcriptome analysis by Next Generation Sequencing integrating the use of unique molecular identifiers.

resultsIPF (median [interquartile range]) was significantly elevated in sepsis patients (6.4 [5.3-8.7] % vs. 3.6 [2.6-4.6] %, p = 0.005). Platelet function testing revealed no differences in adenosine diphosphate- or thrombin receptor activating peptide-induced platelet aggregation between control and sepsis patients. Putative circular RNA transcripts were decreased in platelets from septic patients. Leukocyte contamination defined by CD45 abundance levels in RNA-sequencing was absent in both groups. Principal component analysis of transcripts showed only partial overlap of clustering with IPF levels. RNA sequencing showed up-regulation of 524 and down-regulation of 118 genes in platelets from sepsis patients compared to controls. Upregulated genes were mostly related to catabolic processes and protein translation. Comparison to published platelet transcriptomes showed a large overlap of changes observed in sepsis and COVID-19 but not with reticulated platelets from healthy donors.

conclusionsPatients with sepsis appear to have a less degraded platelet transcriptome as indicated by increased levels of immature platelets and decreased levels of putative circular RNA transcripts. The present data suggests that increased protein translation is a characteristic mechanism of systemic inflammation.

Indexed as

AgedBase SequenceBlood PlateletsCell FractionationGene ExpressionGene Expression ProfilingHumansMalePlatelet ActivationPlatelet AggregationPlatelet Aggregation InhibitorsPlatelet CountPlatelet Function TestsRNA, CircularSepsisSequence Analysis, RNAPlatelet Aggregation InhibitorsRNA, Circular

Identifiers

PMID35085240
PMCPMC8794123
OpenAlexW4210722699

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.