Evidence map›Paper›PMID 26232171›Full record

ArticleBlood2015

Platelets induce apoptosis via membrane-bound FasL.

Rebecca I Schleicher, Frank Reichenbach, Peter Kraft, Anil Kumar, Mario Lescan, Franziska Todt, Kerstin Göbel, Ingo Hilgendorf, Tobias Geisler, Axel Bauer and 11 more

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Blood, 2015. 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 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

51 citing papers in PubMed, 86 citations in OpenAlex.

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  10. Research progress on platelets in glioma.Chinese medical journal · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 10 institutions in 7 countries.

Rebecca I SchleicherDepartment of Cardiovascular Medicine, Section for Cardioimmunology, and Department of Cardiovascular Medicine, University Hospital, Eberhard Karls University, Tuebingen, Germany;
Frank ReichenbachInstitute for Biochemistry and Molecular Biology, Centre for Biochemistry and Molecular Cell Research (ZBMZ), and Faculty of Biology, University of Freiburg, Freiburg, Germany;
Peter KraftDepartment of Neurology, University Hospital Wuerzburg, Wuerzburg, Germany;
Anil KumarNational Eye Institute, Bethesda, MD;
Mario LescanDepartment of Cardiovascular Surgery, University Hospital, Eberhard Karls University, Tuebingen, Germany;
Franziska TodtInstitute for Biochemistry and Molecular Biology, Centre for Biochemistry and Molecular Cell Research (ZBMZ), and.
Kerstin GöbelDepartment of Neurology and Institute of Physiology (Neuropathophysiology), University of Muenster, Muenster, Germany;
Ingo HilgendorfDepartment of Cardiology and Angiology I, Heart Center, University of Freiburg, Freiburg, Germany;
Tobias GeislerDepartment of Cardiovascular Medicine, University Hospital, Eberhard Karls University, Tuebingen, Germany;
Axel BauerDepartment of Cardiovascular Medicine, University Hospital, Eberhard Karls University, Tuebingen, Germany;
Marcus OlbrichDepartment of Cardiovascular Medicine, Section for Cardioimmunology, and Department of Cardiovascular Medicine, University Hospital, Eberhard Karls University, Tuebingen, Germany;
Martin SchallerDepartment of Dermatology, University Hospital, Eberhard Karls University, Tuebingen, Germany;
Sebastian WesselborgInstitute for Molecular Medicine, Heinrich-Heine University Dusseldorf, Dusseldorf, Germany;
Lorraine O'ReillyThe Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia;
Sven G MeuthDepartment of Neurology and Institute of Physiology (Neuropathophysiology), University of Muenster, Muenster, Germany;
Klaus Schulze-OsthoffInterfaculty Institute of Biochemistry, University of Tuebingen, Tuebingen and German Cancer Consortium and German Cancer Research Center, Heidelberg, Germany;
Meinrad GawazDepartment of Cardiovascular Medicine, University Hospital, Eberhard Karls University, Tuebingen, Germany;
Xuri LiState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou, Guangdong, People's Republic of China; and.
Christoph KleinschnitzDepartment of Neurology, University Hospital Wuerzburg, Wuerzburg, Germany;
Frank EdlichInstitute for Biochemistry and Molecular Biology, Centre for Biochemistry and Molecular Cell Research (ZBMZ), and Centre for Biological Signaling Studies, University of Freiburg, Freiburg, Germany.
Harald F LangerDepartment of Cardiovascular Medicine, Section for Cardioimmunology, and Department of Cardiovascular Medicine, University Hospital, Eberhard Karls University, Tuebingen, Germany;
University of Tübingen · DECzech Academy of Sciences, Biology Centre · CZInstitute of Neuroimmunology of the Slovak Academy of Sciences · SKUniversitätsklinikum Würzburg · DEUniversity of Freiburg · DEHeidelberg University · DEHeinrich Heine University Düsseldorf · DENational Eye Institute · USSun Yat-sen University · CNWalter and Eliza Hall Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

After tissue injury, both wound sealing and apoptosis contribute to restoration of tissue integrity and functionality. Although the role of platelets (PLTs) for wound closure and induction of regenerative processes is well established, the knowledge about their contribution to apoptosis is incomplete. Here, we show that PLTs present the death receptor Fas ligand (FasL) on their surface after activation. Activated PLTs as well as the isolated membrane fraction of activated PLTs but not of resting PLTs induced apoptosis in a dose-dependent manner in primary murine neuronal cells, human neuroblastoma cells, and mouse embryonic fibroblasts. Membrane protein from PLTs lacking membrane-bound FasL (FasL(△m/△m)) failed to induce apoptosis. Bax/Bak-mediated mitochondrial apoptosis signaling in target cells was not required for PLT-induced cell death, but increased the apoptotic response to PLT-induced Fas signaling. In vivo, PLT depletion significantly reduced apoptosis in a stroke model and an inflammation-independent model of N-methyl-d-aspartic acid-induced retinal apoptosis. Furthermore, experiments using PLT-specific PF4Cre(+) FasL(fl/fl) mice demonstrated a role of PLT-derived FasL for tissue apoptosis. Because apoptosis secondary to injury prevents inflammation, our findings describe a novel mechanism on how PLTs contribute to tissue homeostasis.

Indexed as

ApoptosisPlatelet ActivationAnimalsBlood PlateletsCells, CulturedFas Ligand ProteinHumansInflammationMice, Inbred C57BLNeuronsStrokeFas Ligand Protein

Identifiers

PMID26232171
PMCPMC4573871
OpenAlexW1157983586

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.