Evidence map›Paper›PMID 30832675›Full record

ArticleCell communication and signaling : CCS2019

Regulation of platelet-activating factor-induced interleukin-8 expression by protein tyrosine phosphatase 1B.

Geneviève Hamel-Côté, Fanny Lapointe, Daniel Gendron, Marek Rola-Pleszczynski, Jana Stankova

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell communication and signaling : CCS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

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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 2 institutions in 1 country.

Geneviève Hamel-CôtéImmunology Division, Department of Pediatrics, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, QC, J1H 4N5, Canada.
Fanny LapointeImmunology Division, Department of Pediatrics, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, QC, J1H 4N5, Canada.
Daniel GendronAgriculture and Agri-Food Canada, Dairy and Swine Research and Development Center, 2000 College Street, Sherbrooke, QC, Canada.
Marek Rola-PleszczynskiImmunology Division, Department of Pediatrics, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, QC, J1H 4N5, Canada.
Jana StankovaImmunology Division, Department of Pediatrics, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, QC, J1H 4N5, Canada. Jana.Stankova@USherbrooke.ca.ORCID 0000-0002-4127-8506
Université de Sherbrooke · CAAgriculture and Agri-Food Canada · CA

Funding

CIHR MOP-142481
6 · The paper itself

Abstract

backgroundPlatelet-activating factor (PAF) is a potent lipid mediator whose involvement in the onset and progression of atherosclerosis is mediated by, among others, the modulation of cytokine expression patterns. The presence of multiple potential protein-tyrosine phosphatase (PTP) 1B substrates in PAF receptor signaling pathways brought us to investigate its involvement in PAF-induced cytokine expression in monocyte-derived dendritic cells (Mo-DCs) and to study the pathways involved in this modulation.

methodsWe used in-vitro-matured human dendritic cells and the HEK-293 cell line in our studies. PTP1B inhibition was though siRNAs and a selective inhibitor. Cytokine expression was studied with RT-PCR, luciferase assays and ELISA. Phosphorylation status of kinases and transcription factors was studied with western blotting.

resultsHere, we report that PTP1B was involved in the modulation of cytokine expression in PAF-stimulated Mo-DCs. A study of the down-regulation of PAF-induced IL-8 expression, by PTP1B, showed modulation of PAF-induced transactivation of the IL-8 promoter which was dependent on the presence of the C/EBPß -binding site. Results also suggested that PTP1B decreased PAF-induced IL-8 production by a glycogen synthase kinase (GSK)-3-dependent pathway via activation of the Src family kinases (SFK). These kinases activated an unidentified pathway at early stimulation times and the PI3K/Akt signaling pathway in a later phase. This change in GSK-3 activity decreased the C/EBPß phosphorylation levels of the threonine 235, a residue whose phosphorylation is known to increase C/EBPß transactivation potential, and consequently modified IL-8 expression.

conclusionThe negative regulation of GSK-3 activity by PTP1B and the consequent decrease in phosphorylation of the C/EBPß transactivation domain could be an important negative feedback loop by which cells control their cytokine production after PAF stimulation.

Indexed as

Binding SitesCCAAT-Enhancer-Binding Protein-betaDendritic CellsGlycogen Synthase Kinase 3HEK293 CellsHumansInterleukin-8Models, BiologicalPhosphorylationPhosphothreoninePlatelet Activating FactorPlatelet Membrane GlycoproteinsPromoter Regions, GeneticProtein Tyrosine Phosphatase, Non-Receptor Type 1Proto-Oncogene Proteins c-aktReceptors, G-Protein-CoupledCCAAT-Enhancer-Binding Protein-betaCEBPB protein, humanGlycogen Synthase Kinase 3Interleukin-8PhosphothreoninePlatelet Activating Factorplatelet activating factor receptorPlatelet Membrane GlycoproteinsProtein Tyrosine Phosphatase, Non-Receptor Type 1Proto-Oncogene Proteins c-aktReceptors, G-Protein-Coupledsrc-Family KinasesCCAAT-enhancer-binding protein(C/EBP)GSK-3Interleukin-8Platelet-activating factorPTP1B

Identifiers

PMID30832675
PMCPMC6399872
OpenAlexW2920264506

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.