Evidence map›Paper›PMID 19632319›Full record

ArticleCellular signalling2009

FcepsilonRI-mediated mast cell migration: signaling pathways and dependence on cytosolic free Ca2+ concentration.

In Duk Jung, Hyun-Sil Lee, Hoi Young Lee, Oksoon Hong Choi

Abstract read
In one paragraph

Article in Cellular signalling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 21 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

4 authors at 2 institutions in 2 countries.

In Duk JungDepartment of Medicine, Division of Allergy and Clinical Immunology, The Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA.
Hyun-Sil Lee
Hoi Young Lee
Oksoon Hong Choi
Johns Hopkins University · USJohns Hopkins Medicine · US

Funding

PI3KC2 Beta in Ca2+ Signaling via Sphingosine KinaseR01HL068879 · NHLBI · MEHARRY MEDICAL COLLEGE · PI CHOI, OKSOON H · 2002 to 2005
$1.0M
NHLBI NIH HHS R01 HL068879NHLBI NIH HHS R01 HL68879
6 · The paper itself

Abstract

IgE-sensitized rat basophilic leukemia (RBL)-2H3 mast cells have been shown to migrate towards antigen. In the present study we tried to identify the mechanism by which antigen causes mast cell migration. Antigen caused migration of RBL-2H3 cells at the concentration ranges of 1000-fold lower than those required for degranulation and the dose response was biphasic. This suggests that mast cells can detect very low concentration gradients of antigen (pg/ml ranges), which initiate migration until they degranulate near the origin of antigen, of which concentration is in the ng/ml ranges. Similar phenomenon was observed in human mast cells (HMCs) derived from CD34(+) progenitors. As one mechanism of mast cell migration, we tested the involvement of sphingosine 1-phosphate (S1P). Fc epsilon RI-mediated cell migration was dependent on the production of S1P but independent of a S1P receptor or its signaling pathways as determined with S1P receptor antagonist VPC23019 and Gi protein inhibitor pertussis toxin (PTX). This indicated that the site of action of S1P produced by antigen stimulation was intracellular. However, S1P-induced mast cell migration was dependent on S1P receptor activation and inhibited by both VPC23019 and PTX. Cell migration towards antigen or extracellular S1P was dependent on the activation of the phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathways, while only migration towards antigen was inhibited by the inhibitors of sphingosine kinase and phospholipase C (PLC) and intracellular calcium chelator BAPTA. In summary, our data suggest that the high affinity receptor for IgE (Fc epsilon RI)-mediated mast cell migration is dependent on the production of S1P but independent of S1P receptors. Cell migration mediated by either Fc epsilon RI or S1P receptors involves activation of both PI3K and MAPK.

Indexed as

AnimalsCalciumCell MovementCells, CulturedEnzyme InhibitorsExtracellular Signal-Regulated MAP KinasesHumansImmunoglobulin ELysophospholipidsMast CellsPertussis ToxinPhosphatidylinositol 3-KinasesRatsReceptors, IgEReceptors, LysosphingolipidSignal TransductionCalciumEnzyme InhibitorsExtracellular Signal-Regulated MAP KinasesImmunoglobulin ELysophospholipidsPertussis ToxinPhosphatidylinositol 3-KinasesReceptors, IgEReceptors, LysosphingolipidSphingosinesphingosine 1-phosphate

Identifiers

PMID19632319
PMCPMC2752894
OpenAlexW2124017874

What OpenQuestion holds

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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.