Evidence map›Paper›PMID 31032885›Full record

ArticleBritish journal of pharmacology2019

Inhibitors of DAG metabolism suppress CCR2 signalling in human monocytes.

Priscilla Day, Lisa Burrows, David Richards, Samuel J Fountain

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 32% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. The human amniotic fluid stem cell secretome triggers intracellular CaJournal of cellular and molecular medicine · 2021
    Article
  3. Article
  4. 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

4 authors at 1 institution in 1 country.

Priscilla DayBiomedical Research Centre, School of Biological Sciences, University of East Anglia, Norwich, UK.
Lisa BurrowsBiomedical Research Centre, School of Biological Sciences, University of East Anglia, Norwich, UK.
David RichardsBiomedical Research Centre, School of Biological Sciences, University of East Anglia, Norwich, UK.
Samuel J FountainBiomedical Research Centre, School of Biological Sciences, University of East Anglia, Norwich, UK.ORCID 0000-0002-6028-0548
University of East Anglia · GB

Funding

British Heart Foundation PG/16/94/32393
6 · The paper itself

Abstract

background and purposeCCL2 is an inflammatory chemokine that stimulates the recruitment of monocytes into tissue via activation of the GPCR CCR2. EXPERIMENTAL APPROACH: Freshly isolated human monocytes and THP-1 cells were used. Fura-2 loaded cells were used to measure intracellular Ca KEY

resultsCCL2 evoked intracellular Ca CONCLUSIONS AND IMPLICATIONS: Taken together, these data suggest that DAG production resulting from CCR2 activation is metabolised by both DAG kinase and DAG lipase pathways in monocytes and that pharmacological inhibition of DAG catabolism or application suppresses signalling on the CCL2-CCR2 axis via a mechanism dependent upon a PKC isoenzyme that is sensitive to Gö6983 but not Gö6976.

Indexed as

CalciumCarbazolesCell MovementChemokine CCL2Diacylglycerol KinaseHumansIndolesLipoprotein LipaseMaleimidesMonocytesProtein Kinase CProtein Kinase InhibitorsReceptors, CCR2Signal TransductionTHP-1 Cells2-(1-(3-dimethylaminopropyl)-5-methoxyindol-3-yl)-3-(1H-indol-3-yl)maleimideCalciumCarbazolesCCR2 protein, humanChemokine CCL2Diacylglycerol KinaseGo 6976IndolesLipoprotein LipaseMaleimidesProtein Kinase CProtein Kinase InhibitorsReceptors, CCR2

Identifiers

PMID31032885
PMCPMC6609539
OpenAlexW2943288826

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.