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PMID:23576987
Citation |
Ge, XN, Ha, SG, Liu, FT, Rao, SP and Sriramarao, P (2013) Eosinophil-expressed galectin-3 regulates cell trafficking and migration. Front Pharmacol 4:37 |
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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. |
Links |
PubMed Online version:10.3389/fphar.2013.00037 |
Keywords |
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Significance
Annotations
Gene product | Qualifier | GO Term | Evidence Code | with/from | Aspect | Extension | Notes | Status |
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GO:0009986: cell surface |
ECO:0000314: |
C |
Gal-3 is known to be expressed on the cell surface of human Eos, but Mouse Eos express Gal-3 as well. Figure 2B shows cell surface expression of Gal-3 in non-permeabilized BM-derived Eos. |
complete | ||||
part_of |
GO:0009986: cell surface |
ECO:0000314: direct assay evidence used in manual assertion |
C |
Seeded From UniProt |
complete | |||
See also
References
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