Evidence map›Paper›PMID 23904157›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

Differential roles of CXCL2 and CXCL3 and their receptors in regulating normal and asthmatic airway smooth muscle cell migration.

Laila A Al-Alwan, Ying Chang, Andrea Mogas, Andrew J Halayko, Carolyn J Baglole, James G Martin, Simon Rousseau, David H Eidelman, Qutayba Hamid

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing 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

83 citing papers in PubMed, 162 citations in OpenAlex.

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  8. Chemokines in Pregnancy.Biomolecules · 2025
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  11. Genomic Locus Tagged by Lung Function GWAS SNV rs12477314 (2q37.3) Acts as a Regulatory Region for a Systemic Inflammatory Phenotype.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
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  15. Article
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23 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 1 country.

Laila A Al-AlwanMeakins-Christie Laboratories and Respiratory Division, Department of Medicine, McGill University, Montreal, Quebec H2X 2P2, Canada.
Ying Chang
Andrea Mogas
Andrew J Halayko
Carolyn J Baglole
James G Martin
Simon Rousseau
David H Eidelman
Qutayba Hamid
Christie (Canada) · CAMcGill University · CAUniversity of Manitoba · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Structural cell migration plays a central role in the pathophysiology of several diseases, including asthma. Previously, we established that IL-17-induced (CXCL1, CXCL2, and CXCL3) production promoted airway smooth muscle cell (ASMC) migration, and consequently we sought to investigate the molecular mechanism of CXC-induced ASMC migration. Recombinant human CXCL1, CXCL2, and CXCL3 were used to assess migration of human primary ASMCs from normal and asthmatic subjects using a modified Boyden chamber. Neutralizing Abs or small interfering RNA (siRNA) knockdown and pharmacological inhibitors of PI3K, ERK1/2, and p38 MAPK pathways were used to investigate the receptors and the signaling pathways involved in CXC-induced ASMC migration, respectively. We established the ability of CXCL2 and CXCL3, but not CXCL1, to induce ASMC migration at the tested concentrations using normal ASMCs. We found CXCL2-induced ASMC migration to be dependent on p38 MAPK and CXCR2, whereas CXCL3-induced migration was dependent on p38 and ERK1/2 MAPK pathways via CXCR1 and CXCR2. While investigating the effect of CXCL2 and CXCL3 on asthmatic ASMC migration, we found that they induced greater migration of asthmatic ASMCs compared with normal ones. Interestingly, unlike normal ASMCs, CXCL2- and CXCL3-induced asthmatic ASMC migration was mainly mediated by the PI3K pathway through CXCR1. In conclusion, our results establish a new role of CXCR1 in ASMC migration and demonstrate the diverse mechanisms by which CXCL2 and CXCL3 mediate normal and asthmatic ASMC migration, suggesting that they may play a role in the pathogenesis of airway remodeling in asthma.

Indexed as

Airway RemodelingAsthmaBlotting, WesternBronchiCell MovementChemokine CXCL1Chemokine CXCL2Chemokines, CXCFlow CytometryHumansMyocytes, Smooth MuscleReceptors, Interleukin-8ARNA, Small InterferingSignal TransductionTransfectionChemokine CXCL1Chemokine CXCL2Chemokines, CXCCXCL2 protein, humanCXCL3 protein, humanReceptors, Interleukin-8ARNA, Small Interfering

Identifiers

PMID23904157
PMCPMC3748335
OpenAlexW2103594524

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.