Evidence map›Paper›PMID 29592875›Full record

ArticleBlood advances2018

Selectins and chemokines use shared and distinct signals to activate β2 integrins in neutrophils.

Tadayuki Yago, Nan Zhang, Liang Zhao, Charles S Abrams, Rodger P McEver

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

40 citing papers in PubMed, 48 citations in OpenAlex.

  1. Trial
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  7. Review
  8. Review
  9. Neutrophils-biology and diversity.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. A humanized βCell reports · 2022
    Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Suppressive Role of Bam32/DAPP1 in Chemokine-Induced Neutrophil Recruitment.International journal of molecular sciences · 2021
    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

5 authors at 3 institutions in 1 country.

Tadayuki YagoCardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK.
Nan ZhangDepartment of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK; and.
Liang ZhaoDepartment of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA.
Charles S AbramsDepartment of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA.
Rodger P McEverCardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK.ORCID 0000-0001-5343-2622
Oklahoma Medical Research Foundation · USUniversity of Pennsylvania · USUniversity of Oklahoma Health Sciences Center · US

Funding

Subcellular Mechanisms pf Platelet ActivationP01HL040387 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI BENNETT, JOEL S. · 1988 to 2018
$35.5M
Thrombosis Models CoreP01HL120846 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI ABRAMS, CHARLES S. · 2014 to 2018
$12.2M
Pilot ProjectP30GM114731 · NIGMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI MCEVER, RODGER PAUL · 2016 to 2020
$6.5M
Signal-dependent neutrophil adhesion to vascular surfacesR01HL034363 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI MCEVER, RODGER PAUL · 1985 to 2017
$3.9M
CYTOPLASMIC REGULATION OF P-SELECTIN/PSGL-1 INTERACTIONSR37HL034363 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI MCEVER, RODGER PAUL · 1998 to 2007
$3.3M
Platelet CLEC-2 regulation of vascular integrity during inflammationR01HL128390 · NHLBI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI MCEVER, RODGER PAUL, XIA, LIJUN · 2016 to 2019
$1.7M
NHLBI NIH HHS P01 HL040387NHLBI NIH HHS P01 HL120846NHLBI NIH HHS R01 HL034363NHLBI NIH HHS R01 HL128390NHLBI NIH HHS R37 HL034363NIGMS NIH HHS P30 GM114731
6 · The paper itself

Abstract

Rolling neutrophils receive signals while engaging P- and E-selectin and chemokines on inflamed endothelium. Selectin signaling activates β2 integrins to slow rolling velocities. Chemokine signaling activates β2 integrins to cause arrest. Despite extensive study, key aspects of these signaling cascades remain unresolved. Using complementary in vitro and in vivo assays, we found that selectin and chemokine signals in neutrophils triggered Rap1a-dependent and phosphatidylinositol-4-phosphate 5-kinase γ (PIP5Kγ90)-dependent pathways that induce integrin-dependent slow rolling and arrest. Interruption of both pathways, but not either pathway alone, blocked talin-1 recruitment to and activation of integrins. An isoform of PIP5Kγ90 lacking the talin-binding domain (PIP5Kγ87) could not activate integrins. Chemokines, but not selectins, used phosphatidylinositol-4,5-bisphosphate 3-kinase γ (PI3Kγ) in cooperation with Rap1a to mediate integrin-dependent slow rolling (at low chemokine concentrations), as well as arrest (at high chemokine concentrations). High levels of chemokines activated β2 integrins without selectin signals. When chemokines were limiting, they synergized with selectins to activate β2 integrins.

Indexed as

Leukocyte RollingAnimalsCD18 AntigensChemokinesClass Ib Phosphatidylinositol 3-KinaseHumansMiceNeutrophilsPhosphotransferases (Alcohol Group Acceptor)rap1 GTP-Binding ProteinsSelectinsSignal Transduction1-phosphatidylinositol-4-phosphate 5-kinaseCD18 AntigensChemokinesClass Ib Phosphatidylinositol 3-KinasePhosphotransferases (Alcohol Group Acceptor)rap1 GTP-Binding ProteinsSelectins

Identifiers

PMID29592875
PMCPMC5894262
OpenAlexW2794911198

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.