Evidence map›Paper›PMID 37993259›Full record

ArticleLife science alliance2024

Megakaryocytes possess a STING pathway that is transferred to platelets to potentiate activation.

Firas El-Mortada, Karima Landelouci, Samuel Bertrand-Perron, Félix-Antoine Aubé, Amélie Poirier, Amel Bidias, Georges Jourdi, Mélanie Welman, Michael P Gantier, Justin R Hamilton and 3 more

Open access · goldAbstract read
In one paragraph

Article in Life science alliance, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. 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

13 authors at 5 institutions in 2 countries.

Firas El-MortadaGroupe de Recherche en Signalisation Cellulaire, Département de Biologie Médicale, Université du Québec à Trois-Rivières, Trois-Rivières, Canada.
Karima LandelouciGroupe de Recherche en Signalisation Cellulaire, Département de Biologie Médicale, Université du Québec à Trois-Rivières, Trois-Rivières, Canada.
Samuel Bertrand-PerronGroupe de Recherche en Signalisation Cellulaire, Département de Biologie Médicale, Université du Québec à Trois-Rivières, Trois-Rivières, Canada.
Félix-Antoine AubéGroupe de Recherche en Signalisation Cellulaire, Département de Biologie Médicale, Université du Québec à Trois-Rivières, Trois-Rivières, Canada.
Amélie PoirierGroupe de Recherche en Signalisation Cellulaire, Département de Biologie Médicale, Université du Québec à Trois-Rivières, Trois-Rivières, Canada.
Amel BidiasGroupe de Recherche en Signalisation Cellulaire, Département de Biologie Médicale, Université du Québec à Trois-Rivières, Trois-Rivières, Canada.ORCID https://orcid.org/0000-0003-1288-3499
Georges JourdiCentre de Recherche, Institut de Cardiologie de Montréal, Montréal, Canada.ORCID https://orcid.org/0000-0001-8738-5975
Mélanie WelmanCentre de Recherche, Institut de Cardiologie de Montréal, Montréal, Canada.
Michael P GantierCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Australia.ORCID https://orcid.org/0000-0003-3740-698X
Justin R HamiltonAustralian Centre for Blood Diseases, Monash University, Melbourne, Australia.
Benjamin KileMonash Biomedicine Discovery Institute and Department of Biochemistry and Molecular Biology, Monash University, Clayton, Australia.ORCID https://orcid.org/0000-0002-8836-8947
Marie LordkipanidzéCentre de Recherche, Institut de Cardiologie de Montréal, Montréal, Canada.ORCID https://orcid.org/0000-0001-7418-6766
Geneviève PépinGroupe de Recherche en Signalisation Cellulaire, Département de Biologie Médicale, Université du Québec à Trois-Rivières, Trois-Rivières, Canada Genevieve.pepin3@uqtr.ca.ORCID https://orcid.org/0000-0001-8625-050X
Université du Québec à Trois-Rivières · CAMontreal Heart Institute · CAAustralian Centre for HIV and Hepatitis Virology Research · AUAustralian Regenerative Medicine Institute · AUHudson Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Platelets display unexpected roles in immune and coagulation responses. Emerging evidence suggests that STING is implicated in hypercoagulation. STING is an adaptor protein downstream of the DNA sensor cyclic GMP-AMP synthase (cGAS) that is activated by cytosolic microbial and self-DNA during infections, and in the context of loss of cellular integrity, to instigate the production of type-I IFN and pro-inflammatory cytokines. To date, whether the cGAS-STING pathway is present in platelets and contributes to platelet functions is not defined. Using a combination of pharmacological and genetic approaches, we demonstrate here that megakaryocytes and platelets possess a functional cGAS-STING pathway. Our results suggest that in megakaryocytes, STING stimulation activates a type-I IFN response, and during thrombopoiesis, cGAS and STING are transferred to proplatelets. Finally, we show that both murine and human platelets contain cGAS and STING proteins, and the cGAS-STING pathway contributes to potentiation of platelet activation and aggregation. Taken together, these observations establish for the first time a novel role of the cGAS-STING DNA sensing axis in the megakaryocyte and platelet lineage.

Indexed as

Interferon Type IMegakaryocytesAnimalsCytokinesDNAHumansMiceNucleotidyltransferasesSignal TransductionCytokinesDNAInterferon Type INucleotidyltransferases

Identifiers

PMID37993259
PMCPMC10665521
OpenAlexW4388906326

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.