Evidence map›Paper›PMID 27482114›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

CCN1/CYR61-mediated meticulous patrolling by Ly6Clow monocytes fuels vascular inflammation.

Beat A Imhof, Stephane Jemelin, Romain Ballet, Christian Vesin, Marc Schapira, Melis Karaca, Yalin Emre

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. 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 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing 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

37 citing papers in PubMed, 72 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Beat A ImhofDepartment of Pathology and Immunology, University of Geneva, 1205 Geneva, Switzerland;
Stephane JemelinDepartment of Pathology and Immunology, University of Geneva, 1205 Geneva, Switzerland;
Romain BalletDepartment of Pathology and Immunology, University of Geneva, 1205 Geneva, Switzerland;
Christian VesinDepartment of Physiology and Metabolism, University of Geneva, 1205 Geneva, Switzerland.
Marc SchapiraDepartment of Pathology and Immunology, University of Geneva, 1205 Geneva, Switzerland;
Melis KaracaDepartment of Physiology and Metabolism, University of Geneva, 1205 Geneva, Switzerland.
Yalin EmreDepartment of Pathology and Immunology, University of Geneva, 1205 Geneva, Switzerland; yalinemre@gmail.com.
University of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation is characterized by the recruitment of leukocytes from the bloodstream. The rapid arrival of neutrophils is followed by a wave of inflammatory lymphocyte antigen 6 complex (Ly6C)-positive monocytes. In contrast Ly6C(low) monocytes survey the endothelium in the steady state, but their role in inflammation is still unclear. Here, using confocal intravital microscopy, we show that upon Toll-like receptor 7/8 (TLR7/8)-mediated inflammation of mesenteric veins, platelet activation drives the rapid mobilization of Ly6C(low) monocytes to the luminal side of the endothelium. After repeatedly interacting with platelets, Ly6C(low) monocytes commit to a meticulous patrolling of the endothelial wall and orchestrate the subsequent arrival and extravasation of neutrophils through the production of proinflammatory cytokines and chemokines. At a molecular level, we show that cysteine-rich protein 61 (CYR61)/CYR61 connective tissue growth factor nephroblastoma overexpressed 1 (CCN1) protein is released by activated platelets and enables the recruitment of Ly6C(low) monocytes upon vascular inflammation. In addition endothelium-bound CCN1 sustains the adequate patrolling of Ly6C(low) monocytes both in the steady state and under inflammatory conditions. Blocking CCN1 or platelets with specific antibodies impaired the early arrival of Ly6C(low) monocytes and abolished the recruitment of neutrophils. These results refine the leukocyte recruitment cascade model by introducing endothelium-bound CCN1 as an inflammation mediator and by demonstrating a role for platelets and patrolling Ly6C(low) monocytes in acute vascular inflammation.

Indexed as

AnimalsAntigens, LyBlood PlateletsCell MovementCysteine-Rich Protein 61MiceMice, Inbred C57BLMonocytesNeutrophilsToll-Like Receptor 7Toll-Like Receptor 8VasculitisAntigens, LyCCN1 protein, mouseCysteine-Rich Protein 61Ly-6C antigen, mouseToll-Like Receptor 7Toll-Like Receptor 8CCN1inflammationmonocyteneutrophilplatelet

Identifiers

PMID27482114
PMCPMC4995973
OpenAlexW2476500174

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.