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

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

Autor Gil, C. D. Google Scholar
La, M. Google Scholar
Perretti, M. Google Scholar
Oliani, S. M. Google Scholar
Instituição UNESP
Universidade Federal de São Paulo (UNIFESP)
Universidade de São Paulo (USP)
Queen Mary Sch Med & Dent
Resumo 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. (c) 2006 International Federation for Cell Biology. Published by Elsevier B.V. All rights reserved.
Palavra-chave annexin
galectin
Ea.hy926 cells
transmigration assay
immunogold electron microscopy
Idioma Inglês
Data de publicação 2006-04-01
Publicado em Cell Biology International. London: Academic Press Ltd Elsevier B.V., v. 30, n. 4, p. 338-344, 2006.
ISSN 1065-6995 (Sherpa/Romeo, fator de impacto)
Publicador Elsevier B.V.
Extensão 338-344
Fonte http://dx.doi.org/10.1016/j.cellbi.2005.12.010
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000237186000007
Endereço permanente http://repositorio.unifesp.br/handle/11600/28811

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