The E-selectin-ligand ESL-1 is located in the Golgi as well as on microvilli on the cell surface

Abstract

Neutrophils and subsets of lymphocytes bind to E-selectin, a cytokine inducible adhesion molecule on endothelial cells. The E-selectin-ligand-1 (ESL-1) is a high affinity glycoprotein ligand which participates in the binding of mouse myeloid cells to E-selectin. The sequence of mouse ESL-1 is highly homologous to the cysteine rich FGF receptor (CFR) in chicken and the rat Golgi protein MG160. We have analysed the subcellular distribution of ESL-1 by indirect immunofluorescence, flow cytometry, various biochemical techniques and by immunogold scanning electron microscopy. We could localize ESL-1 in the Golgi as well as on the cell surface of 32Dc13 cells and neutrophils. Cell surface staining was confirmed by cell surface biotinylation and by cell surface immunoprecipitations in which antibodies only had access to surface proteins on intact cells. In addition, ESL-1(high) and ESL-1(low) expressing cells, sorted by flow cytometry, gave rise to high and low immunoprecipitation signals for ESL-1, respectively. Based on immunogold labeling of intact cells, we localized ESL-1 on microvilli of 32Dc13 cells and of the lymphoma cell line K46. Quantitative evaluation determined 80% of the total labeling for ESL-1 on microvilli of K46 cells while 69% of the labeling for the control antigen B220 was found on the planar cell surface. These data indicate that ESL-1 occurs at sites on the leukocyte cell surface which are destined for the initiation of cell contacts to the endothelium.

Protein Markers of Ischemic Insult in Brain Endothelial Cells Identified Using 2D Gel Electrophoresis and ICAT-Based Quantitative Proteomics

“…The up-regulation of both membrane-bound and soluble E-selectin has been extensively documented (100 literature entries) in brain vascular system for its role in leukocyte rolling and recruitment in ischemic brain disease. In contrast, the up-regulation of E-selectin ligand-1, a major binding partner of E-selectin expressed by myeloid cells and not previously described in endothelial cells, was observed in both the cellular fraction of RBEC in vitro and in ischemic brain vessels in vivo . The functional role of this protein in inflammatory endothelial responses to ischemia remains unknown.…”

Antitumor effect of memantine is related to the formation of the splicing isoform of GLG1, a decoy FGF‑binding protein

“…The present study observed a change in the protein and mRNA expression of GLG1. The function of GLG1 and its different variants has been reported in several studies (35,(40)(41)(42)45,53,63,73). The aim of the present study was to report these phenomena.…”

“…In particular, GLG1 is a 160-kDa membrane sialoglycoprotein, originally isolated from the Golgi apparatus of rat neurons (32,33). Two homologs, the chicken cysteine-rich fibroblast growth factor receptor (CFR) (34) and ESL-1 (35)(36)(37), were identified in embryonic chick and murine myeloid cells, respectively. This FGF-binding protein has 16 cysteine-rich repeats in the extracellular luminal amino-terminal region, 21 amino acids in the transmembrane domain, and 13 amino acids in the intracellular cytoplasmic carboxy-terminal domain (Fig.…”

“…1B). GLG1 is a conserved membrane sialoglycoprotein of the Golgi apparatus in the majority of cells, displaying >90% amino acid sequence identity with CFR (30) and ESL-1 (30,31,(33)(34)(35)39). The GLG1 gene was assigned to human chromosome 16q22-23 (40).…”

N-metil-3,4 metilenodioximetanfetamina (MDMA - Ecstasy) diminui a resposta imune inata e a resistência à Listeria monocytogenes: papel do eixo HPA e do sistema nervoso simpático

“…(ICAM e VCAM) na superfície luminal dos vasos, que se ligam em seus receptores expressos constutivamente na membrana de neutrófilos (P-selectina ligante 1, Eselectina ligante 1 e L-selectina) promovendo o rolamento e o primeiro contato dos neutrófilos com as células endoteliais (Farsky e Mello, 1995;Farsky,Sannomiya e Garcia-Leme, 1995;Bruehl et al, 1997;Steegmaier et al, 1997;Buscher et al, 2010). Durante este contato inicial ocorre a ativação de vias de sinalização nos neutrófilos que regulam uma forte adesão entre as moléculas de adesão expressas nos neutrófilos (LFA-1 e Mac-1) e os seus ligantes (ICAM-1 e ICAM-2) expressos no endotélio ativado, diminuindo a velocidade de rolamento e permitindo a transmigração destas células até o foco inflamatório (Bunting et al, 2002).…”