Evidence map›Paper›PMID 27055904›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2016

P2Y12 Receptor Modulates Sepsis-Induced Inflammation.

Elisabetta Liverani, Mario C Rico, Alexander Y Tsygankov, Laurie E Kilpatrick, Satya P Kunapuli

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

64 citing papers in PubMed, 97 citations in OpenAlex.

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  8. Impact of Estrogen on Purinergic Signaling in Microvascular Disease.International journal of molecular sciences · 2025
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  15. Platelet P2YBritish journal of pharmacology · 2024
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  17. Lung protective effect of Ticagrelor in endotoxemia.Journal of medicine and life · 2023
    Article
  18. The Signaling Pathway of the ADP Receptor P2YInternational journal of molecular sciences · 2023
    Review
  19. Article
  20. The ATP-dependent Pathways and Human Diseases.Current medicinal chemistry · 2023
    Article

4 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Elisabetta LiveraniFrom the Sol Sherry Thrombosis Research Center (E.L., M.C.R., A.Y.T., L.E.K., S.P.K.), Department of Physiology (L.E.K., S.P.K.), Department of Microbiology and Immunology (A.Y.T.), and Center for Inflammation, Translational and Clinical Lung Research (E.L., L.E.K.), Temple University School of Medicine, Philadelphia, PA. eliliverani@temple.edu.
Mario C RicoFrom the Sol Sherry Thrombosis Research Center (E.L., M.C.R., A.Y.T., L.E.K., S.P.K.), Department of Physiology (L.E.K., S.P.K.), Department of Microbiology and Immunology (A.Y.T.), and Center for Inflammation, Translational and Clinical Lung Research (E.L., L.E.K.), Temple University School of Medicine, Philadelphia, PA.
Alexander Y TsygankovFrom the Sol Sherry Thrombosis Research Center (E.L., M.C.R., A.Y.T., L.E.K., S.P.K.), Department of Physiology (L.E.K., S.P.K.), Department of Microbiology and Immunology (A.Y.T.), and Center for Inflammation, Translational and Clinical Lung Research (E.L., L.E.K.), Temple University School of Medicine, Philadelphia, PA.
Laurie E KilpatrickFrom the Sol Sherry Thrombosis Research Center (E.L., M.C.R., A.Y.T., L.E.K., S.P.K.), Department of Physiology (L.E.K., S.P.K.), Department of Microbiology and Immunology (A.Y.T.), and Center for Inflammation, Translational and Clinical Lung Research (E.L., L.E.K.), Temple University School of Medicine, Philadelphia, PA.
Satya P KunapuliFrom the Sol Sherry Thrombosis Research Center (E.L., M.C.R., A.Y.T., L.E.K., S.P.K.), Department of Physiology (L.E.K., S.P.K.), Department of Microbiology and Immunology (A.Y.T.), and Center for Inflammation, Translational and Clinical Lung Research (E.L., L.E.K.), Temple University School of Medicine, Philadelphia, PA.
Temple University · US

Funding

Functional PKC Isoforms in PlateletsR01HL093231 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI KUNAPULI, SATYA P. · 2009 to 2017
$3.6M
Regulation and function of PDK1-Akt-Pyk2 axis in plateletsR01HL118593 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI KUNAPULI, SATYA P. · 2013 to 2016
$1.9M
Novel Protein Kinase C Targeted Therapy for Acute Lung InjuryR01HL111552 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI KILPATRICK, LAURIE E · 2012 to 2015
$1.5M
Molecular Mechanisms of the Increased Cardiovascular Risk in Rheumatoid ArthritisK01HL103197 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI RICO, MARIO CESAR · 2010 to 2014
$701k
NHLBI NIH HHS K01 HL103197NHLBI NIH HHS R01 HL093231NHLBI NIH HHS R01 HL111552NHLBI NIH HHS R01 HL118593
6 · The paper itself

Abstract

objectivePlatelets modulate hemostasis and immune responses via interactions with immune cells through secretion of immunemodulators and cell-cell interactions. The P2Y12 receptor mediates ADP-induced aggregation and secretion in platelets. APPROACH AND

resultsUsing a mouse model of intra-abdominal sepsis and acute lung injury, we investigated the role of the P2Y12 receptor in neutrophil migration and lung inflammation in P2Y12 null mice and in mice pretreated with the P2Y12 antagonist clopidogrel. Our data show a decrease in circulating white blood cells and a decrease in platelet activation and platelet-leukocyte interactions in treated mice compared with untreated mice. Additionally, lung injury and platelet sequestration were diminished in clopidogrel-treated mice compared with their untreated septic littermates. Similar results were observed in P2Y12 null mice: platelet activation and platelet-leukocyte aggregates were decreased in septic P2Y12 null mice compared with wild-type mice. P2Y12 null mice were refractory to lung injury compared with wild-type mice. Finally, to evaluate P2Y12-independent effects of clopidogrel, we pretreated P2Y12 null mice. Interestingly, the number of circulating neutrophils was reduced in treated septic P2Y12 null mice, suggesting neutrophils as a target for clopidogrel pleiotropic effects. No difference was observed in P2Y1 null mice during sepsis, indicating that the P2Y12 receptor is responsible for the effects.

conclusionsP2Y12 null mice are refractory to sepsis-induced lung injury, suggesting a key role for activated platelets and the P2Y12 receptor during sepsis.

Indexed as

Platelet ActivationAcute Lung InjuryAnimalsBlood PlateletsClopidogrelCytokinesGenetic Predisposition to DiseaseLeukocytesLungMaleMice, Inbred C57BLMice, KnockoutNeutrophil InfiltrationPhenotypePlatelet Aggregation InhibitorsPneumoniaClopidogrelCytokinesP2ry12 protein, mousePlatelet Aggregation InhibitorsP-SelectinPurinergic P2Y Receptor AntagonistsReceptors, Purinergic P2Y12Ticlopidineacute lung injuryneutrophilsP2Y12 receptorplateletssepsis

Identifiers

PMID27055904
PMCPMC4850113
OpenAlexW2327347746

What OpenQuestion holds

Textmetadata
LicenceTDM
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.