Interaction of human neutrophils with endothelial cells regulates the expression of endogenous proteins annexin 1, galectin-1 and galectin-3

Authors

  • Cristiane Damas Gil,

    1. Post-Graduation in Morphology, São Paulo School of Medicine—UNIFESP, São Paulo (SP), Brazil
    2. Department of Anatomy, Faculty of Medicine (FAMERP), São José do Rio Preto (SP), Brazil
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  • Mylinh La,

    1. The William Harvey Research Institute, Queen Mary School of Medicine and Dentistry, London, UK
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  • Mauro Perretti,

    1. The William Harvey Research Institute, Queen Mary School of Medicine and Dentistry, London, UK
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  • Sonia Maria Oliani

    Corresponding author
    1. Department of Biology, Instituto de Biociências, Letras e Ciências Exatas (IBILCE), University of São Paulo State (UNESP), São José do Rio Preto (SP), Brazil
    2. Post-Graduation in Morphology, São Paulo School of Medicine—UNIFESP, São Paulo (SP), Brazil
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Corresponding author. Department of Biology, IBILCE-UNESP, Rua Cristóvão Colombo 2265, CEP 15054-000, São José do Rio Preto (SP), Brazil. Tel.: +55 17 3221 2381; fax: +55 17 3221 2390. smoliani@ibilce.unesp.br

Abstract

Annexin 1 (ANXA1), galectin-1 (Gal-1) and galectin-3 (Gal-3) proteins have been identified as important mediators that promote or inhibit leukocyte migration. The expression of these proteins was studied in human neutrophils and endothelial cells (ECs) during a transmigration process induced by IL-8. Upon neutrophil adhesion to EC, a significant increase in the cleaved ANXA1 (LCS3, raised against all ANXA1 isoforms) expression was detected in the plasma membrane of adhered neutrophils and ECs compared to intact ANXA1 isoform (LCPS1, against N-terminus of protein). Adherent neutrophils had elevated Gal-3 levels in the nucleus and cytoplasm, and ECs in their plasma membranes. In contrast, a decrease in the total amounts of Gal-1 was detected in migrated compared to non-migrated neutrophils. Therefore, ANXA1 and Gal-3 changed in their content and localization when neutrophils adhere to endothelia, suggesting a process of sensitive-balance between two endogenous anti- and pro-inflammatory mediators.

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