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Eosinophil-expressed galectin-3 regulates cell trafficking and migration

Overview of attention for article published in Frontiers in Pharmacology, January 2013
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Title
Eosinophil-expressed galectin-3 regulates cell trafficking and migration
Published in
Frontiers in Pharmacology, January 2013
DOI 10.3389/fphar.2013.00037
Pubmed ID
Authors

Xiao Na Ge, Sung Gil Ha, Fu-Tong Liu, Savita P. Rao, P. Sriramarao

Abstract

Galectin-3 (Gal-3), a β galactoside-binding lectin, is implicated in the pathogenesis of allergic airway inflammation and allergen-challenged mice deficient in Gal-3 (Gal-3(-/-)) exhibit decreased airway recruitment of eosinophils (Eos). Gal-3 is expressed and secreted by several cell types and can thus function extracellularly and intracellularly to regulate a variety of cellular responses. We sought to determine the role of Eos-expressed Gal-3 in promoting Eos trafficking and migration in the context of allergic airway inflammation using bone marrow (BM)-derived Eos from wild-type (WT) and Gal-3(-/-) mice. Airway recruitment of Eos in acute (4 weeks) and chronic (8-12 weeks) allergen-challenged WT mice correlated with Gal-3 expression in the lungs. BM-derived Eos were found to express Gal-3 on the cell surface and secrete soluble Gal-3 when exposed to eotaxin-1. Compared to WT Eos, Gal-3(-/-) Eos exhibited significantly reduced rolling on vascular cell adhesion molecule 1 (VCAM-1) and decreased stable adhesion on intercellular adhesion molecule 1 (ICAM-1) under conditions of flow in vitro. Evaluation of cytoskeletal rearrangement demonstrated that relatively fewer adherent Gal-3(-/-) Eos undergo cell spreading and formation of membrane protrusions. In addition, cell surface expression of integrin receptor αM (CD11b) was lower in Gal-3(-/-) Eos, which is likely to account for their altered adhesive interactions with VCAM-1 and ICAM-1. Gal-3(-/-) Eos also exhibited significantly decreased migration toward eotaxin-1 compared to WT Eos irrespective of similar levels of CCR3 expression. Further, eotaxin-induced migration of WT Eos remained unaffected in the presence of lactose, suggesting a role for intracellular Gal-3 in regulating Eos migration. Overall, our findings indicate that Gal-3 expression in the lungs correlates with Eos mobilization during allergic airway inflammation and signaling involving intracellular Gal-3 and/or secreted Gal-3 bound to the cell surface of Eos appears to be essential for Eos trafficking under flow as well as for migration.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 20 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Turkey 1 5%
Unknown 19 95%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 6 30%
Researcher 5 25%
Other 1 5%
Professor 1 5%
Lecturer 1 5%
Other 2 10%
Unknown 4 20%
Readers by discipline Count As %
Agricultural and Biological Sciences 9 45%
Medicine and Dentistry 3 15%
Immunology and Microbiology 2 10%
Biochemistry, Genetics and Molecular Biology 1 5%
Veterinary Science and Veterinary Medicine 1 5%
Other 0 0%
Unknown 4 20%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 05 April 2013.
All research outputs
#20,189,002
of 22,705,019 outputs
Outputs from Frontiers in Pharmacology
#9,913
of 15,930 outputs
Outputs of similar age
#248,733
of 280,712 outputs
Outputs of similar age from Frontiers in Pharmacology
#92
of 167 outputs
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We're also able to compare this research output to 167 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.