Evidence map›Paper›PMID 25405900›Full record

ArticlePloS one2014

Regulator of G-protein signaling 18 controls both platelet generation and function.

Nathalie Delesque-Touchard, Caroline Pendaries, Cécile Volle-Challier, Laurence Millet, Véronique Salel, Caroline Hervé, Anne-Marie Pflieger, Laurence Berthou-Soulie, Catherine Prades, Tania Sorg and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. A regulatory node involving GαJournal of thrombosis and haemostasis : JTH · 2023
    Article
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  18. Negative regulators of platelet activation and adhesion.Journal of thrombosis and haemostasis : JTH · 2018
    Review
  19. Platelets at the Vascular Interface.Research and practice in thrombosis and haemostasis · 2018
    Article
  20. Article
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 2 institutions in 1 country.

Nathalie Delesque-TouchardEarly to Candidate (E2C), Sanofi, Toulouse, France.
Caroline PendariesEarly to Candidate (E2C), Sanofi, Toulouse, France.
Cécile Volle-ChallierEarly to Candidate (E2C), Sanofi, Toulouse, France.
Laurence MilletEarly to Candidate (E2C), Sanofi, Toulouse, France.
Véronique SalelEarly to Candidate (E2C), Sanofi, Toulouse, France.
Caroline HervéEarly to Candidate (E2C), Sanofi, Toulouse, France.
Anne-Marie PfliegerEarly to Candidate (E2C), Sanofi, Toulouse, France.
Laurence Berthou-SoulieSCP Biologics, Sanofi, Vitry-Sur-Seine, France.
Catherine PradesSCP Biologics, Sanofi, Vitry-Sur-Seine, France.
Tania SorgDepartment of Scientific Operations PhenoPro, Mouse Clinical Institute (MCI), Strasbourg, France.
Jean-Marc HerbertEarly to Candidate (E2C), Sanofi, Toulouse, France.
Pierre SaviEarly to Candidate (E2C), Sanofi, Toulouse, France.
Françoise BonoEarly to Candidate (E2C), Sanofi, Toulouse, France.
Sanofi (France) · FRInstitut Clinique de la Souris · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RGS18 is a myeloerythroid lineage-specific regulator of G-protein signaling, highly expressed in megakaryocytes (MKs) and platelets. In the present study, we describe the first generation of a RGS18 knockout mouse model (RGS18-/-). Interesting phenotypic differences between RGS18-/- and wild-type (WT) mice were identified, and show that RGS18 plays a significant role in both platelet generation and function. RGS18 deficiency produced a gain of function phenotype in platelets. In resting platelets, the level of CD62P expression was increased in RGS18-/- mice. This increase correlated with a higher level of plasmatic serotonin concentration. RGS18-/- platelets displayed a higher sensitivity to activation in vitro. RGS18 deficiency markedly increased thrombus formation in vivo. In addition, RGS18-/- mice presented a mild thrombocytopenia, accompanied with a marked deficit in MK number in the bone marrow. Analysis of MK maturation in vitro and in vivo revealed a defective megakaryopoiesis in RGS18-/- mice, with a lower bone marrow content of only the most committed MK precursors. Finally, RGS18 deficiency was correlated to a defect of platelet recovery in vivo under acute conditions of thrombocytopenia. Thus, we highlight a role for RGS18 in platelet generation and function, and provide additional insights into the physiology of RGS18.

Indexed as

Analysis of VarianceAnimalsBlood Cell CountFlow CytometryMegakaryocytesMiceMice, Inbred C57BLMice, KnockoutPhylogenyPlatelet ActivationPromoter Regions, GeneticRGS ProteinsSerotoninSignal TransductionThrombosisRgs18 protein, mouseRGS ProteinsSerotonin

Identifiers

PMID25405900
PMCPMC4236145
OpenAlexW2001181206

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.