Sulfated Glycolipids Are Ligands for a Lymphocyte Homing Receptor, L-Selectin (LECAM-1), Binding Epitope in Sulfated Sugar Chain

Suzuki, Yoshiyuki; Toda, Yoshihisa; Tamatani, Takuya; Watanabe, Toshiaki; Suzuki, Tadashi; Nakao, Toshiko; Murase, Ken; Kiso, Maki; Hasegawa, Asako; Tadano-Aritomi, Keiko; Ishizuka, Ineo; Miyasaka, Masayuki

doi:10.1006/bbrc.1993.1065

Cited by 139 publications

(70 citation statements)

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“…Subsequently, cell death was assessed by trypan blue staining (a). Staining with Annexin V and 7-AAD was also performed to detect early apoptotic (Annexin V L-selectin ligands, 35 and examined the changes in CXCR4 expression. Sulfatide induced a significant increase in surface CXCR4 expression on neutrophils (Figure 6d-f) and shedding of L-selectin (Figure 6g and h).…”

Section: Activation Of Cxcr4 By Cxcl12 Attenuated Cell Death Of Isolamentioning

confidence: 99%

The increase in surface CXCR4 expression on lung extravascular neutrophils and its effects on neutrophils during endotoxin-induced lung injury

Yamada

Kubo

Kobayashi³

et al. 2011

Cell Mol Immunol

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Inflammatory stimuli, such as a microbes or lipopolysaccharides, induce a rapid release of neutrophils from the bone marrow and promote neutrophil migration into inflamed sites to promote host defense. However, an excess accumulation and retention of neutrophils in inflamed tissue can cause severe tissue injuries in the later stages of inflammation. Recent studies have reported that both CXCL12 levels in injured lungs and its receptor, CXCR4, on accumulated neutrophils in injured lungs, increased; furthermore, these studies showed that the CXCL12/CXCR4 signaling pathway participated in neutrophil accumulation in the later stages of lipopolysaccharide (LPS)-induced lung injury. However, the mechanisms underlying this increase in surface CXCR4 expression in neutrophils remain unclear. In this study, we found that surface CXCR4 expression increased in extravascular, but not intravascular, neutrophils in the lungs of LPS-induced lung injury model mice. Furthermore, ex vivo studies revealed that CXCL12 acted not only as a chemoattractant, but also as a suppressor of cell death for the lung neutrophils expressing CXCR4. Sulfatide, one of the native ligands for L-selectin, induced the increase of surface CXCR4 expression on isolated circulating neutrophils, suggesting that the activation of L-selectin may be involved in the increase in surface CXCR4. Our findings show that surface CXCR4 levels on neutrophils increase after extravasation into injured lungs, possibly through the activation of L-selectin. The CXCL12/CXCR4 signaling pathway plays an important role in the modulation of neutrophil activity during acute lung injury, not only by promoting chemotaxis but also by suppressing cell death.

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Section: Activation Of Cxcr4 By Cxcl12 Attenuated Cell Death Of Isolamentioning

confidence: 99%

The increase in surface CXCR4 expression on lung extravascular neutrophils and its effects on neutrophils during endotoxin-induced lung injury

Yamada

Kubo

Kobayashi³

et al. 2011

Cell Mol Immunol

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“…Sulfated glycosphingolipids are known to bind specifically to diverse adhesion proteins such as laminin, selectins, and anti-coagulant factors in vitro (9). For example, Suzuki et al (24) reported that L-selectin binds to SM4, SM3, SB2, and SB1a. These facts imply that secreted or cell surface galectin-4 may also modulate the interaction of these proteins with sulfated glycosphingolipids, because galectin-4 interacts with the membrane through adhesion to sulfated glycosphingolipids.…”

Section: Immobilized Galectin-4 Bound To Cck-81 Cells Through 3-osulfmentioning

confidence: 99%

Galectin-4 Binds to Sulfated Glycosphingolipids and Carcinoembryonic Antigen in Patches on the Cell Surface of Human Colon Adenocarcinoma Cells

Ideo

Seko

Yamashita

2005

Journal of Biological Chemistry

104

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Galectin-4, a member of the galectin family, is expressed in the epithelium of the alimentary tract. It has two tandemly repeated carbohydrate recognition domains and specifically binds to an SO 3 ؊ 33Gal␤133GalNAc pyranoside with high affinity (Ideo, H., Seko, A., Ohkura, T., Matta, K. L., and Yamashita, K. (2002) Glycobiology 12, 199-208). In this study, we found that galectin-4 binds to glycosphingolipids carrying 3-O-sulfated Gal residues, such as SB1a, SM3, SM4s, SB2, SM2a, and GM1, but not to glycosphingolipids with 3-O-sialylated Gal, such as sLc4Cer, snLc4Cer, GM3, GM2, and GM4, using both an enzyme-linked immunosorbent assay and a surface plasmon resonance assay. A confocal immunocytochemical assay showed that galectin-4 was colocalized with SB1a, GM1, and carcinoembryonic antigen (CEA) in the patches on the cell surface of human colon adenocarcinoma CCK-81 and LS174T cells. This localization was distinct from caveolin/VIP21 localization. Furthermore, immobilized galectin-4 promoted adhesion of CCK-81 cells through the sulfated glycosphingolipid, SB1a. CEA also bound to galectin-4 with K D value of 2 ؋ 10 ؊8 M by surface plasmon resonance and coimmunoprecipitated with galectin-4 in LS174T cell lysates. These findings suggest that SB1a and CEA in the patches on the cell surface of human colon adenocarcinoma cells could be biologically important ligands for galectin-4.

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“…Sulfatide has been shown to be a natural ligand for L-selectin, P-selectin and galectin-4 [10][11][12]. The signaling induced by sulfatide was shown to activate NF-jB through L-selectin [13], but was also reported to activate leukocytes through an L-selectin-independent pathway [14].…”

Section: Introductionmentioning

confidence: 99%

Up‐regulation of leukocyte CXCR4 expression by sulfatide: An L‐selectin‐dependent pathway on CD4⁺ T cells

et al. 2007

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CXCR4 plays significant roles in immune and inflammatory responses and is important for selective recruitment of leukocytes. We previously showed that CXCR4 surface expression of human lymphocytes was affected by sulfatide, an in vivo ligand for L-selectin. Increased CXCR4 expression was shown to promote biologically relevant functions such as integrin-dependent adhesion and transmigration. Here, we show that sulfatide-induced CXCR4 up-regulation also occurs on other leukocyte subsets in humans and mice. B cells and CD4 + CD25 + T cells had the highest CXCR4 up-regulation after sulfatide stimulation. Transfection of L-selectin was sufficient for K562 cells to acquire sulfatide-induced CXCR4 up-regulation, while analysis of L-selectin knockout mice revealed that this response was critically L-selectin dependent only for CD4 + T cells, suggesting an alternative pathway in CD8 + T cells and B cells. Sulfatide triggered several intracellular signaling events in CD4 + T cells, but only tyrosine kinase activation, including members of the Src family, were essential for L-selectin to CXCR4 signaling. CXCR4 up-regulation was rapid, enhanced CXCL12-induced signaling and increased chemotaxis toward CXCL12, and therefore has potentially important roles in vivo. Thus, the response to CXCL12 depends in part on tissue expression of sulfatide and, specifically in CD4 + T cells, also depends on the surface level of L-selectin.

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Sulfated Glycolipids Are Ligands for a Lymphocyte Homing Receptor, L-Selectin (LECAM-1), Binding Epitope in Sulfated Sugar Chain

Cited by 139 publications

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The increase in surface CXCR4 expression on lung extravascular neutrophils and its effects on neutrophils during endotoxin-induced lung injury

The increase in surface CXCR4 expression on lung extravascular neutrophils and its effects on neutrophils during endotoxin-induced lung injury

Galectin-4 Binds to Sulfated Glycosphingolipids and Carcinoembryonic Antigen in Patches on the Cell Surface of Human Colon Adenocarcinoma Cells

Up‐regulation of leukocyte CXCR4 expression by sulfatide: An L‐selectin‐dependent pathway on CD4⁺ T cells

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Sulfated Glycolipids Are Ligands for a Lymphocyte Homing Receptor, L-Selectin (LECAM-1), Binding Epitope in Sulfated Sugar Chain

Cited by 139 publications

References 0 publications

The increase in surface CXCR4 expression on lung extravascular neutrophils and its effects on neutrophils during endotoxin-induced lung injury

The increase in surface CXCR4 expression on lung extravascular neutrophils and its effects on neutrophils during endotoxin-induced lung injury

Galectin-4 Binds to Sulfated Glycosphingolipids and Carcinoembryonic Antigen in Patches on the Cell Surface of Human Colon Adenocarcinoma Cells

Up‐regulation of leukocyte CXCR4 expression by sulfatide: An L‐selectin‐dependent pathway on CD4+ T cells

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Up‐regulation of leukocyte CXCR4 expression by sulfatide: An L‐selectin‐dependent pathway on CD4⁺ T cells