ArticlePloS one2021
Galectin-1 and platelet factor 4 (CXCL4) induce complementary platelet responses in vitro.
Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Galectin-1 in Cardiovascular Pathogenesis: Unraveling Dual Roles and Mechanistic Insights in Emerging Research.Medicina (Kaunas, Lithuania) · 2025Review
- Review
- Thymidine phosphorylase mediates SARS-CoV-2 spike protein enhanced thrombosis in K18-hACE2Thrombosis research · 2024Article
- Article
- Platelets regulate ischemia-induced revascularization and angiogenesis by secretion of growth factor-modulating factors.Blood advances · 2023Article
- Chemokine Heteromers and Their Impact on Cellular Function-A Conceptual Framework.International journal of molecular sciences · 2023Review
- The interplay of galectins-1, -3, and -9 in the immune-inflammatory response underlying cardiovascular and metabolic disease.Cardiovascular diabetology · 2022Review
- Galectokines: The Promiscuous Relationship between Galectins and Cytokines.Biomolecules · 2022Review
- Galectin 1-A Key Player between Tissue Repair and Fibrosis.International journal of molecular sciences · 2022Review
- Chemokines modulate glycan binding and the immunoregulatory activity of galectins.Communications biology · 2021Article
- Combined Antiplatelet Therapy Reduces the Proinflammatory Properties of Activated Platelets.TH open : companion journal to thrombosis and haemostasis · 2021Article
- Rapid Internalization and Nuclear Translocation of CCL5 and CXCL4 in Endothelial Cells.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Galectin-1 (gal-1) is a carbohydrate-binding lectin with important functions in angiogenesis, immune response, hemostasis and inflammation. Comparable functions are exerted by platelet factor 4 (CXCL4), a chemokine stored in the α-granules of platelets. Previously, gal-1 was found to activate platelets through integrin αIIbβ3. Both gal-1 and CXCL4 have high affinities for polysaccharides, and thus may mutually influence their functions. The aim of this study was to investigate a possible synergism of gal-1 and CXCL4 in platelet activation. Platelets were treated with increasing concentrations of gal-1, CXCL4 or both, and aggregation, integrin activation, P-selectin and phosphatidyl serine (PS) exposure were determined by light transmission aggregometry and by flow cytometry. To investigate the influence of cell surface sialic acid, platelets were treated with neuraminidase prior to stimulation. Gal-1 and CXCL4 were found to colocalize on the platelet surface. Stimulation with gal-1 led to integrin αIIbβ3 activation and to robust platelet aggregation, while CXCL4 weakly triggered aggregation and primarily induced P-selectin expression. Co-incubation of gal-1 and CXCL4 potentiated platelet aggregation compared with gal-1 alone. Whereas neither gal-1 and CXCL4 induced PS-exposure on platelets, prior removal of surface sialic acid strongly potentiated PS exposure. In addition, neuraminidase treatment increased the binding of gal-1 to platelets and lowered the activation threshold for gal-1. However, CXCL4 did not affect binding of gal-1 to platelets. Taken together, stimulation of platelets with gal-1 and CXCL4 led to distinct and complementary activation profiles, with additive rather than synergistic effects.
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