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Journal articles on the topic 'L-selectin'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Peng, Shuang, Shen-Bao Chen, Lin-Da Li, et al. "Impact of real-time shedding on binding kinetics of membrane-remaining L-selectin to PSGL-1." American Journal of Physiology-Cell Physiology 316, no. 5 (2019): C678—C689. http://dx.doi.org/10.1152/ajpcell.00212.2018.

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L-selectin shedding induced by various cytokines is crucial in activating neutrophils (PMNs) in inflammatory cascade. While the real-time shedding in vivo lasts ~10 min after PMN activation, the impact of time-dependent shedding on binding kinetics of membrane-remaining L-selectins to its ligands is poorly understood at transient or steady state. Here, we developed an in vitro L-selectin shedding dynamics approach, together with competitive assays of cell adhesion, and proposed a theoretical model for quantifying the impact of real-time shedding on the binding kinetics of membrane-remaining L-

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2

Mattila, Polly E., Chad E. Green, Ulrich Schaff, Scott I. Simon, and Bruce Walcheck. "Cytoskeletal interactions regulate inducible L-selectin clustering." American Journal of Physiology-Cell Physiology 289, no. 2 (2005): C323—C332. http://dx.doi.org/10.1152/ajpcell.00603.2004.

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L-selectin (CD62L) amplifies neutrophil capture within the microvasculature at sites of inflammation. Activation by G protein-coupled stimuli or through ligation of L-selectin promotes clustering of L-selectin and serves to increase its adhesiveness, signaling, and colocalization with β2-integrins. Currently, little is known about the molecular process regulating the lateral mobility of L-selectin. On neutrophil stimulation, a progressive change takes place in the organization of its plasma membrane, resulting in membrane domains that are characteristically enriched in glycosyl phosphatidylino

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3

Miles, Mary P., Sharyn K. Leach, William J. Kraemer, Keiichiro Dohi, Jill A. Bush, and Andrea M. Mastro. "Leukocyte adhesion molecule expression during intense resistance exercise." Journal of Applied Physiology 84, no. 5 (1998): 1604–9. http://dx.doi.org/10.1152/jappl.1998.84.5.1604.

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We hypothesized that expression of L-selectin and very late antigen-4 (VLA-4) integrin adhesion molecules would influence cell type-specific redistribution during exercise. Women subjects performed six sets of 10-repetition maximum squats. L-selectin and VLA-4 integrin were measured by using flow cytometry pre- and postexercise on peripheral blood neutrophils and lymphocytes ( n = 29 subjects) and lymphocyte subsets ( n = 70 subjects), respectively. Neutrophil concentration increased 41.8% ( P < 0.001), whereas the percent expressing L-selectin was unchanged (79%). Lymphocyte concentration

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4

Alon, R., R. C. Fuhlbrigge, E. B. Finger, and T. A. Springer. "Interactions through L-selectin between leukocytes and adherent leukocytes nucleate rolling adhesions on selectins and VCAM-1 in shear flow." Journal of Cell Biology 135, no. 3 (1996): 849–65. http://dx.doi.org/10.1083/jcb.135.3.849.

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We demonstrate an additional step and a positive feedback loop in leukocyte accumulation on inflamed endothelium. Leukocytes in shear flow bind to adherent leukocytes through L-selectin/ligand interactions and subsequently bind downstream and roll on inflamed endothelium, purified E-selectin, P-selectin, L-selectin, VCAM-1, or peripheral node addressin. Thus adherent leukocytes nucleate formation of strings of rolling cells and synergistically enhance leukocyte accumulation. Neutrophils, monocytes, and activated T cell lines, but not peripheral blood T lymphocytes, tether to each other through

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5

Nelson, RM, O. Cecconi, WG Roberts, A. Aruffo, RJ Linhardt, and MP Bevilacqua. "Heparin oligosaccharides bind L- and P-selectin and inhibit acute inflammation." Blood 82, no. 11 (1993): 3253–58. http://dx.doi.org/10.1182/blood.v82.11.3253.3253.

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Abstract Initial attachment of leukocytes to the vessel wall at sites of inflammation is supported by a family of carbohydrate-binding adhesion molecules called the selectins. Selectin ligands include sialyl-Lewis x (sLex, Neu5Ac alpha 2–3Gal beta 1–4[Fuc alpha 1–3]GlcNAc--) and related structures. We report here that defined heparin oligosaccharides interact with the selectins. Heparin chains containing four or more monosaccharide residues inhibited the function of L- and P-selectin, but not E-selectin, in vitro. In a competition enzyme-linked immunosorbent assay measuring inhibition of solut

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6

Nelson, RM, O. Cecconi, WG Roberts, A. Aruffo, RJ Linhardt, and MP Bevilacqua. "Heparin oligosaccharides bind L- and P-selectin and inhibit acute inflammation." Blood 82, no. 11 (1993): 3253–58. http://dx.doi.org/10.1182/blood.v82.11.3253.bloodjournal82113253.

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Initial attachment of leukocytes to the vessel wall at sites of inflammation is supported by a family of carbohydrate-binding adhesion molecules called the selectins. Selectin ligands include sialyl-Lewis x (sLex, Neu5Ac alpha 2–3Gal beta 1–4[Fuc alpha 1–3]GlcNAc--) and related structures. We report here that defined heparin oligosaccharides interact with the selectins. Heparin chains containing four or more monosaccharide residues inhibited the function of L- and P-selectin, but not E-selectin, in vitro. In a competition enzyme-linked immunosorbent assay measuring inhibition of solution-phase

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7

Matala, Erik, Shelia R. Alexander, Takashi K. Kishimoto, and Bruce Walcheck. "The Cytoplasmic Domain of L-Selectin Participates in Regulating L-Selectin Endoproteolysis." Journal of Immunology 167, no. 3 (2001): 1617–23. http://dx.doi.org/10.4049/jimmunol.167.3.1617.

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8

Jutila, M. A., G. Watts, B. Walcheck, and G. S. Kansas. "Characterization of a functionally important and evolutionarily well-conserved epitope mapped to the short consensus repeats of E-selectin and L-selectin." Journal of Experimental Medicine 175, no. 6 (1992): 1565–73. http://dx.doi.org/10.1084/jem.175.6.1565.

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Selectins represent a new family of adhesion molecules, expressed by leukocytes and endothelial cells, that are involved in the regulation of leukocyte traffic. Here we have characterized a new monoclonal antibody (mAb) (EL-246) that recognizes both human leukocyte L-selectin (previously called LAM-1, LECAM-1, or gp90MEL-14) and endothelial cell E-selectin (previously called ELAM-1). EL-246 recognized a 110-kD protein expressed on cells transfected with E-selectin cDNA and stained many postcapillary venules in inflamed human tonsil. EL-246 also stained human peripheral blood leukocytes and sho

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9

Alon, Ronen, Shuqi Chen, Kamal D. Puri, Erik B. Finger, and Timothy A. Springer. "The Kinetics of L-selectin Tethers and the Mechanics of Selectin-mediated Rolling." Journal of Cell Biology 138, no. 5 (1997): 1169–80. http://dx.doi.org/10.1083/jcb.138.5.1169.

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Two mechanisms have been proposed for regulating rolling velocities on selectins. These are (a) the intrinsic kinetics of bond dissociation, and (b) the reactive compliance, i.e., the susceptibility of the bond dissociation reaction to applied force. To determine which of these mechanisms explains the 7.5–11.5-fold faster rolling of leukocytes on L-selectin than on E- and P-selectins, we have compared the three selectins by examining the dissociation of transient tethers. We find that the intrinsic kinetics for tether bond dissociation are 7–10-fold more rapid for L-selectin than for E- and P-

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10

Dwir, Oren, Geoffrey S. Kansas, and Ronen Alon. "Cytoplasmic anchorage of L-selectin controls leukocyte capture and rolling by increasing the mechanical stability of the selectin tether." Journal of Cell Biology 155, no. 1 (2001): 145–56. http://dx.doi.org/10.1083/jcb.200103042.

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L-selectin is a leukocyte lectin that mediates leukocyte capture and rolling in the vasculature. The cytoplasmic domain of L-selectin has been shown to regulate leukocyte rolling. In this study, the regulatory mechanisms by which this domain controls L-selectin adhesiveness were investigated. We report that an L-selectin mutant generated by truncation of the COOH-terminal 11 residues of L-selectin tail, which impairs association with the cytoskeletal protein α-actinin, could capture leukocytes to glycoprotein L-selectin ligands under physiological shear flow. However, the conversion of initial

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11

MALHOTRA, Rajneesh, Neil R. TAYLOR, and Michael I. BIRD. "Anionic phospholipids bind to L-selectin (but not E-selectin) at a site distinct from the carbohydrate-binding site." Biochemical Journal 314, no. 1 (1996): 297–303. http://dx.doi.org/10.1042/bj3140297.

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It is known that L-selectin binds to glycoconjugates containing the tetrasaccharide sialyl Lewis X in a Ca2+-dependent manner. In addition, a number of other acidic oligosaccharides (for example heparin or chondroitin sulphate) or glycolipids (for example sulphatides) bind to L-selectin independent of cations. In this paper we have established that L-selectin binds to charged phospholipids, such as cardiolipin and phosphatidylserine, but not to neutral phospholipids such as phosphatidylcholine. No interaction between E-selectin and any phospholipid was observed. The interaction between L-selec

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12

Mowery, Patricia, Zhi-Qiang Yang, Eva J. Gordon, et al. "Synthetic Glycoprotein Mimics Inhibit L-Selectin-Mediated Rolling and Promote L-Selectin Shedding." Chemistry & Biology 11, no. 5 (2004): 725–32. http://dx.doi.org/10.1016/j.chembiol.2004.03.027.

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13

Foxall, C., SR Watson, D. Dowbenko, et al. "The three members of the selectin receptor family recognize a common carbohydrate epitope, the sialyl Lewis(x) oligosaccharide." Journal of Cell Biology 117, no. 4 (1992): 895–902. http://dx.doi.org/10.1083/jcb.117.4.895.

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The selectins (lectin-EGF-complement binding-cell adhesion molecules [LEC-CAMs]) are a family of mammalian receptors implicated in the initial interactions between leukocytes and vascular endothelia, leading to lymphocyte homing, platelet binding, and neutrophil extravasation. The three known selectins, L-selectin (leukocyte adhesion molecule-1 [LECAM-1]), E-selectin (endothelial-leukocyte adhesion molecule-1 [ELAM-1]), and P-selectin (GMP-140) share structural features that include a calcium-dependent lectin domain. The sialyl Lewis(x) carbohydrate epitope has been reported as a ligand for bo

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14

Li, Ying, Jennifer Brazzell, Amy Herrera, and Bruce Walcheck. "ADAM17 deficiency by mature neutrophils has differential effects on L-selectin shedding." Blood 108, no. 7 (2006): 2275–79. http://dx.doi.org/10.1182/blood-2006-02-005827.

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Abstract L-selectin directs neutrophils to sites of inflammation, and upon their activation, surface expression of the receptor is rapidly down-regulated by ectodomain shedding. Tumor necrosis factor–α–converting enzyme (TACE, or ADAM17) is a sheddase of L-selectin; however, Adam17 gene targeting (ADAM17ΔZn/ΔZn) in mice is perinatal lethal and its role in L-selectin shedding by mature neutrophils has not been determined. This was addressed here by using radiation-chimeric mice reconstituted with ADAM17ΔZn/ΔZn fetal liver cells. ADAM17-deficient neutrophils, monocytes, and lymphocytes failed to

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15

Haznedaroğlu, I. C., M. Benekli, M. C. Savaş, I. H. Güllū, S. V. Dündar, and Ş. Kirazli. "Serum L-Selectin and P-Selectin levels in lymphomas." European Journal of Cancer 33 (September 1997): S268. http://dx.doi.org/10.1016/s0959-8049(97)86122-9.

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16

Haznedaroğlu, I. C., I. H. Güllü, M. C. Savaş, et al. "Serum L-selectin and P-selectin levels in lymphomas." Haematologia 30, no. 1 (2000): 27–30. http://dx.doi.org/10.1163/15685590051129841.

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17

Bélanger, Simon D., and Yves St-Pierre. "Role of selectins in the triggering, growth, and dissemination of T-lymphoma cells: implication of L-selectin in the growth of thymic lymphoma." Blood 105, no. 12 (2005): 4800–4806. http://dx.doi.org/10.1182/blood-2004-04-1406.

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Abstract We previously showed that intercellular adhesion molecule-1 (ICAM-1) expression by the host is essential for lymphoma dissemination. Because selectins usually act in a coordinated fashion with ICAM-1 in the recruitment of circulating normal cells, we investigated their implication in lymphomagenesis and metastasis. Using selectin-deficient mice, we found that though the absence of E-, P-, or L-selectins did not affect the triggering of radiation-induced thymic lymphoma, the absence of L-selectin on lymphoma cells reduced their capacity to grow in the thymus. This defect, however, was

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18

Xu, J., I. S. Grewal, G. P. Geba, and R. A. Flavell. "Impaired primary T cell responses in L-selectin-deficient mice." Journal of Experimental Medicine 183, no. 2 (1996): 589–98. http://dx.doi.org/10.1084/jem.183.2.589.

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L-selectin is a homing receptor that mediates the selective attachment of leukocytes to specialized high endothelial venules. To study the potential role of L-selectin in immune responses in intact mice, we generated L-selectin-deficient mice by gene targeting. L-selectin-deficient mice are defective in cutaneous delayed-type hypersensitivity (DTH) responses when tested after conventional intervals of immunization (4 d). Primary T cell proliferative responses and cytokine production (interleukin [IL] 2, IL-4, and interferon gamma) were also compromised when tested after 5 d of immunization, in

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19

Spertini, O., A. S. Cordey, N. Monai, L. Giuffrè, and M. Schapira. "P-selectin glycoprotein ligand 1 is a ligand for L-selectin on neutrophils, monocytes, and CD34+ hematopoietic progenitor cells." Journal of Cell Biology 135, no. 2 (1996): 523–31. http://dx.doi.org/10.1083/jcb.135.2.523.

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Selectins play a critical role in initiating leukocyte binding to vascular endothelium. In addition, in vitro experiments have shown that neutrophils use L-selectin to roll on adherent neutrophils, suggesting that they express a nonvascular L-selectin ligand. Using a L-selectin/IgM heavy chain (mu) chimeric protein as an immunocytological probe, we show here that L-selectin can bind to neutrophils, monocytes, CD34+ hematopoietic progenitors, and HL-60 and KG-1 myeloid cells. The interaction between L-selectin and leukocytes was protease sensitive and calcium dependent, and abolished by cell tr

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20

Shigeta, Akiko, Masanori Matsumoto, Thomas F. Tedder, John B. Lowe, Masayuki Miyasaka, and Takako Hirata. "An L-selectin ligand distinct from P-selectin glycoprotein ligand-1 is expressed on endothelial cells and promotes neutrophil rolling in inflammation." Blood 112, no. 13 (2008): 4915–23. http://dx.doi.org/10.1182/blood-2008-04-153866.

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Abstract Neutrophils recruited from the blood are key players in the innate immune response. Selectins play critical roles in neutrophil recruitment by mediating their tethering and rolling in inflamed venules. While the roles of P- and E-selectin in this process are well established, the mechanisms of L-selectin–mediated neutrophil recruitment remain elusive. One proposal is that tethering is mediated by L-selectin on flowing neutrophils interacting with P-selectin glycoprotein ligand-1 (PSGL-1) on adherent neutrophils. To clarify whether L-selectin–mediated neutrophil recruitment depends ent

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21

Corsi, M. M., D. Pagani, G. Dogliotti, F. Perona, G. Sambataro, and L. Pignataro. "Protein Biochip Array of Adhesion Molecule Expression in Peripheral Blood of Patients with Nasal Polyposis." International Journal of Biological Markers 23, no. 2 (2008): 115–20. http://dx.doi.org/10.1177/172460080802300208.

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Nasal polyposis is a chronic non-infectious inflammatory disease of the nasal and paranasal cavity mucosa of unknown multifactorial origin in which inflammatory cells, and in particular eosinophils, seem to play a pivotal role. Eosinophil migration from the bloodstream to nasal polyps is considered to be specific and is a complex process involving several different molecules such as ICAM-1, VCAM-1, and L-, P- and E-selectins. The aim of this study was to investigate, using a protein biochip array technology, the concentrations of these molecules in the peripheral blood of a group of patients a

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22

von Andrian, UH, JD Chambers, EL Berg, et al. "L-selectin mediates neutrophil rolling in inflamed venules through sialyl LewisX-dependent and -independent recognition pathways." Blood 82, no. 1 (1993): 182–91. http://dx.doi.org/10.1182/blood.v82.1.182.bloodjournal821182.

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The glycoprotein (GP) L-selectin initiates adhesive interactions between leukocytes and endothelial cells (EC). It functions as a lymphocyte-lectin homing receptor recognizing carbohydrate determinants of the peripheral lymph node addressing on high endothelial venules. It also mediates neutrophil rolling, the earliest interaction of neutrophils with acutely inflamed venules. Neutrophil L-selectin presents sialyl-LewisX (sLe(X)) as a ligand to P- and E-selectin in vitro, and we have proposed that this is a major mechanism of L- selectin-mediated rolling in vivo. In contrast, the contribution o

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23

Thomas, Susan N., Ronald L. Schnaar, and Konstantinos Konstantopoulos. "Podocalyxin-like protein is an E-/L-selectin ligand on colon carcinoma cells: comparative biochemical properties of selectin ligands in host and tumor cells." American Journal of Physiology-Cell Physiology 296, no. 3 (2009): C505—C513. http://dx.doi.org/10.1152/ajpcell.00472.2008.

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Selectins facilitate metastasis and tumor cell arrest in the microvasculature by mediating binding of selectin-expressing host cells to ligands on tumor cells. We recently identified CD44 variant isoforms as functional P-, but not E-/L-, selectin ligands on colon carcinoma cells. Furthermore, a ∼180-kDa sialofucosylated glycoprotein(s) mediated selectin binding in CD44-knockdown cells. Using immunoaffinity chromatography and tandem mass spectrometry, we identify podocalyxin-like protein (PCLP) as an alternative selectin ligand. Blot rolling and cell-free flow-based adhesion assays disclose tha

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24

Abbal, Claire, Martine Lambelet, Debora Bertaggia, et al. "Lipid raft adhesion receptors and Syk regulate selectin-dependent rolling under flow conditions." Blood 108, no. 10 (2006): 3352–59. http://dx.doi.org/10.1182/blood-2006-04-013912.

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Abstract Selectins and their ligand P-selectin glycoprotein ligand-1 (PSGL-1) mediate leukocyte rolling along inflamed vessels. Cell rolling is modulated by selectin interactions with their ligands and by topographic requirements including L-selectin and PSGL-1 clustering on tips of leukocyte microvilli. Lipid rafts are cell membrane microdomains reported to function as signaling platforms. Here, we show that disruption of leukocyte lipid rafts with cholesterol chelating agents depleted raft-associated PSGL-1 and L-selectin and strongly reduced L-, P-, and E-selectin–dependent rolling. Cholest

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25

Rosen, Steven D. "Homing in on L-Selectin." Journal of Immunology 177, no. 1 (2006): 3–4. http://dx.doi.org/10.4049/jimmunol.177.1.3.

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26

Rosen, Steven D. "Endothelial Ligands for L-Selectin." American Journal of Pathology 155, no. 4 (1999): 1013–20. http://dx.doi.org/10.1016/s0002-9440(10)65201-7.

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27

Stamenkovic, Ivan. "The L-selectin adhesion system." Current Opinion in Hematology 2, no. 1 (1995): 68–75. http://dx.doi.org/10.1097/00062752-199502010-00010.

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28

Waddell, Thomas K., Lea Fialkow, Chi Kin Chan, Takashi Kei Kishimoto, and Gregory P. Downey. "Signaling Functions of L-selectin." Journal of Biological Chemistry 270, no. 25 (1995): 15403–11. http://dx.doi.org/10.1074/jbc.270.25.15403.

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29

Martinez, Manuel, Magali Joffraud, Sylvain Giraud, et al. "Regulation of PSGL-1 Interactions with L-selectin, P-selectin, and E-selectin." Journal of Biological Chemistry 280, no. 7 (2004): 5378–90. http://dx.doi.org/10.1074/jbc.m410899200.

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30

MALHOTRA, Rajneesh, Malcolm WARD, Robert B. SIM, and Michael I. BIRD. "Identification of human complement Factor H as a ligand for L-selectin." Biochemical Journal 341, no. 1 (1999): 61–69. http://dx.doi.org/10.1042/bj3410061.

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The selectin family of adhesion molecules (E-, P- and L-selectins) is involved in leukocyte recruitment to sites of inflammation and tissue damage. Recently it has been shown that L-selectin is involved not only in leukocyte tethering and rolling, but also plays an important role in leukocyte activation. For example, glycosylation-dependent cell-adhesion molecule 1 (GlyCAM-1), a known ligand for L-selectin, has been shown to enhance β2-integrin function. GlyCAM-1 is a secreted protein and is present in mouse serum at a concentration of approx. 1.5 μg/ml. There is no obvious GlyCAM-1 homologue

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31

Berg, Ellen L., John Magnani, R. Aaron Warnock, Martyn K. Robinson, and Eugene C. Butcher. "Comparison of L-selectin and E-selectin ligand specificities: The L-selectin can bind the E-selectin ligands Sialyl Lex and Sialyl Lea." Biochemical and Biophysical Research Communications 184, no. 2 (1992): 1048–55. http://dx.doi.org/10.1016/0006-291x(92)90697-j.

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32

Hafezi-Moghadam, Ali, Kennard L. Thomas, Alyson J. Prorock, Yuqing Huo, and Klaus Ley. "L-Selectin Shedding Regulates Leukocyte Recruitment." Journal of Experimental Medicine 193, no. 7 (2001): 863–72. http://dx.doi.org/10.1084/jem.193.7.863.

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The physiologic role of L-selectin shedding is unknown. Here, we investigate the effect of L-selectin shedding on firm adhesion and transmigration. In a tumor necrosis factor α–induced model of inflammation, inhibition of L-selectin shedding significantly increased firm adhesion and transmigration by a lymphocyte function–associated antigen (LFA)-1 and intercellular adhesion molecule (ICAM)-1–dependent mechanism. We examined the quality of leukocyte rolling and L-selectin–mediated signaling. Blockade of L-selectin shedding significantly reduced the “jerkiness” of leukocyte rolling, defined as

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33

Zoldhelyi, Pierre, Pamela J. Beck, Robert J. Bjercke, et al. "Inhibition of coronary thrombosis and local inflammation by a noncarbohydrate selectin inhibitor." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 6 (2000): H3065—H3075. http://dx.doi.org/10.1152/ajpheart.2000.279.6.h3065.

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We tested the hypothesis that selectin inhibition with blocking antibodies or a small-molecular-weight inhibitor of L-, P-, and E-selectin, methoxybenzoylpropionic acid (MBPA), prevents thrombus formation in a canine coronary Folts' model. Cyclic flow variations (CFVs) were induced by crush injury and constriction of the left anterior descending coronary artery in dogs. Systemic infusion of antibodies to P- and L-selectin abolished CFVs, respectively, in 50% and 17% of treated dogs [ P = not significant (NS)]. The combination of P- and L-selectin antibodies suppressed CFVs in 60% of treated do

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34

Furie, Barbara, Bruce Furie, and Jing Yang. "The Biology of P-Selectin Glycoprotein Ligand-1: Its Role as a Selectin Counterreceptor in Leukocyte-Endothelial and Leukocyte-Platelet Interaction." Thrombosis and Haemostasis 81, no. 01 (1999): 1–7. http://dx.doi.org/10.1055/s-0037-1614407.

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SummaryCell-cell interactions mediating leukocyte trafficking, thrombogene-sis and inflammation are crucial for the host defense mechanism. The selectin family of integral membrane proteins includes E-selectin, L-selectin and P-selectin. Selectins mediate tethering and rolling of leukocytes to the vessel wall at the site of inflammation. The counter-receptor for P-selectin and possibly the other selectins is P-selectin glycoprotein ligand-1 (PSGL-1). This review focuses on the properties and biology of PSGL-1.

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35

Armstead, V. E., A. G. Minchenko, R. A. Schuhl, R. Hayward, T. O. Nossuli, and A. M. Lefer. "Regulation of P-selectin expression in human endothelial cells by nitric oxide." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 2 (1997): H740—H746. http://dx.doi.org/10.1152/ajpheart.1997.273.2.h740.

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P-selectin translocation to the surface of endothelial cells is increased after exposure to the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME), resulting in increased endothelial adhesiveness. L-NAME (3 mM) was added to human cultured iliac vein endothelial cells for 1, 2, 4, and 6 h, and P-selectin mRNA expression was quantified by a ribonuclease protection assay. In parallel experiments, the NO donor, SPM-5185 (10 microM), was added to human iliac venous endothelial cells, and P-selectin mRNA expression quantified. P-selectin protein synthesis was quantified b

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36

Crockett-Torabi, E., and J. C. Fantone. "L-selectin stimulation of canine neutrophil initiates calcium signal secondary to tyrosine kinase activation." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 3 (1997): H1302—H1308. http://dx.doi.org/10.1152/ajpheart.1997.272.3.h1302.

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Neutrophils play an important role in myocardial ischemia-reperfusion injury. Neutrophil adhesion to the vascular endothelium is one of the important early mechanisms that lead to reperfusion injury. The leukocyte adhesion molecule, L-selectin, plays a major role in the initial interaction between neutrophils and endothelial cells. Intervention aimed at blocking selectins or their associated ligands can exert cardioprotective effects. The purpose of this study was to examine the role of L-selectin in the initiation of transmembrane signaling and regulation of canine neutrophil responses. Cross

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37

Darwish, Iman, Yevgeniy Brailovsky, Amir Darki, et al. "Dysregulation of Hemostatic Biomarkers, Inflammatory Biomarkers, and Alteration of Cellular Indices As Predictors of Adverse Outcomes in Pulmonary Embolism Patients." Blood 134, Supplement_1 (2019): 2408. http://dx.doi.org/10.1182/blood-2019-126876.

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Background: Pulmonary Embolism (PE) is a condition that affects a multitude of individuals worldwide. The pathophysiology of PE is multifactorial and complex. Measuring levels of biomarkers in PE patient plasma may be predictive of patient outcomes in terms of survival, and such biomarkers could be correlated to other parameters such as white cell counts and their ratios. Adhesion molecules, such as selectins, have been predicted to play a role in the pathophysiology of PE, however their relationship to other cellular parameters is not fully explored. P-selectin is found on platelets, and is i

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38

Lawrence, Michael B., Geoffrey S. Kansas, Eric J. Kunkel, and Klaus Ley. "Threshold Levels of Fluid Shear Promote Leukocyte Adhesion through Selectins (CD62L,P,E)." Journal of Cell Biology 136, no. 3 (1997): 717–27. http://dx.doi.org/10.1083/jcb.136.3.717.

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Leukocyte adhesion through L-selectin to peripheral node addressin (PNAd, also known as MECA-79 antigen), an L-selectin ligand expressed on high endothelial venules, has been shown to require a minimum level of fluid shear stress to sustain rolling interactions (Finger, E.B., K.D. Puri, R. Alon, M.B. Lawrence, V.H. von Andrian, and T.A. Springer. 1996. Nature (Lond.). 379:266–269). Here, we show that fluid shear above a threshold of 0.5 dyn/cm2 wall shear stress significantly enhances HL-60 myelocyte rolling on P- and E-selectin at site densities of 200/μm2 and below. In addition, gravitationa

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Houshmand, B., A. Rafiei, M. Hajilooi, K. Mani-Kashani, and L. Gholami. "E-selectin and L-selectin polymorphisms in patients with periodontitis." Journal of Periodontal Research 44, no. 1 (2009): 88–93. http://dx.doi.org/10.1111/j.1600-0765.2008.01092.x.

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Dimitroff, Charles J., Jack Y. Lee, Kenneth S. Schor, Brenda M. Sandmaier, and Robert Sackstein. "Differential L-Selectin Binding Activities of Human Hematopoietic Cell L-Selectin Ligands, HCELL and PSGL-1." Journal of Biological Chemistry 276, no. 50 (2001): 47623–31. http://dx.doi.org/10.1074/jbc.m105997200.

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Expression of L-selectin on human hematopoietic cells (HC) is associated with a higher proliferative activity and a more rapid engraftment after hematopoietic stem cell transplantation. Two L-selectin ligands are expressed on human HCs, P-selectin glycoprotein ligand-1 (PSGL-1) and a specialized glycoform of CD44 (hematopoietic cell E- and L-selectin ligand, HCELL). Although the structural biochemistry of HCELL and PSGL-1 is well characterized, the relative capacity of these molecules to mediate L-selectin-dependent adhesion has not been explored. In this study, we examined under shear stress

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Nolte, D., P. Schmid, U. Jager, et al. "Leukocyte rolling in venules of striated muscle and skin is mediated by P-selectin, not by L-selectin." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 4 (1994): H1637—H1642. http://dx.doi.org/10.1152/ajpheart.1994.267.4.h1637.

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Leukocyte rolling in post-capillary venules is mediated by adhesion molecules of the selectin family expressed on both leukocytes (L-selectin) and endothelial cells (E- and P-selectin). With the use of intravital fluorescence microscopy, the effects of antibodies against these selectins were analyzed in the skinfold chamber model of BALB/c mice and the ear model of homozygous hairless mice (hr/hr) that permit chronic observation of striated muscle and skin microcirculation in awake animals, respectively. Mice were injected intravenously with monoclonal antibodies (MAb) to murine L-selectin and

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Collins, Robert G., Unsu Jung, Maricela Ramirez, et al. "Dermal and pulmonary inflammatory disease in E-selectin and P-selectin double-null mice is reduced in triple-selectin–null mice." Blood 98, no. 3 (2001): 727–35. http://dx.doi.org/10.1182/blood.v98.3.727.

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Abstract In the initial phase of an inflammatory response, leukocytes marginate and roll along the endothelial surface as a result of adhesive interactions between molecules on the endothelial cells and leukocytes. To evaluate the role of the 3 selectins (E, L, and P) in leukocyte rolling and emigration, a null mutation for L-selectin was introduced into previously described embryonic stem cells with null mutations in the genes for both E-selectin and P-selectin (E/P double mutants) to produce triple-selectin–null mice (E-selectin, L-selectin, and P-selectin [E/L/P] triple mutants). Triple-sel

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Collins, Robert G., Unsu Jung, Maricela Ramirez, et al. "Dermal and pulmonary inflammatory disease in E-selectin and P-selectin double-null mice is reduced in triple-selectin–null mice." Blood 98, no. 3 (2001): 727–35. http://dx.doi.org/10.1182/blood.v98.3.727.h8000727_727_735.

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In the initial phase of an inflammatory response, leukocytes marginate and roll along the endothelial surface as a result of adhesive interactions between molecules on the endothelial cells and leukocytes. To evaluate the role of the 3 selectins (E, L, and P) in leukocyte rolling and emigration, a null mutation for L-selectin was introduced into previously described embryonic stem cells with null mutations in the genes for both E-selectin and P-selectin (E/P double mutants) to produce triple-selectin–null mice (E-selectin, L-selectin, and P-selectin [E/L/P] triple mutants). Triple-selectin hom

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Kansas, GS, KB Saunders, K. Ley, et al. "A role for the epidermal growth factor-like domain of P-selectin in ligand recognition and cell adhesion." Journal of Cell Biology 124, no. 4 (1994): 609–18. http://dx.doi.org/10.1083/jcb.124.4.609.

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The selectin family of adhesion molecules mediates the initial interactions of leukocytes with endothelium. The extracellular region of each selectin contains an amino-terminal C-type lectin domain, followed by an EGF-like domain and multiple short consensus repeat units (SCR). Previous studies have indirectly suggested a role for each of the extracellular domains of the selectins in cell adhesion. In this study, a panel of chimeric selectins created by exchange of domains between L- and P-selectin was used to directly examine the role of the extracellular domains in cell adhesion. Exchange of

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Ivetic, A., and A. J. Ridley. "The telling tail of L-selectin." Biochemical Society Transactions 32, no. 6 (2004): 1118–21. http://dx.doi.org/10.1042/bst0321118.

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L-selectin is constitutively expressed on the surface of most leucocytes and is important for tethering and subsequent rolling of leucocytes on endothelial cells, facilitating their migration into secondary lymphoid organs (e.g. naive T cells) and sites of inflammation (e.g. neutrophils). Previous studies have shown that the 17-amino-acid L-selectin cytoplasmic tail is important for its function in cell adhesion and, hence, identifying binding partners will provide insight into how L-selectin is regulated in leucocytes. This review describes currently known binding partners of the L-selectin t

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Evans, Sharon S., Wan-Chao Wang, Mark D. Bain, Randy Burd, Julie R. Ostberg, and Elizabeth A. Repasky. "Fever-range hyperthermia dynamically regulates lymphocyte delivery to high endothelial venules." Blood 97, no. 9 (2001): 2727–33. http://dx.doi.org/10.1182/blood.v97.9.2727.

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Abstract Fever is associated with increased survival during acute infection, although its mechanism of action is largely unknown. This study found evidence of an unexpectedly integrated mechanism by which fever-range temperatures stimulate lymphocyte homing to secondary lymphoid tissues by increasing L-selectin and α4β7 integrin–dependent adhesive interactions between circulating lymphocytes and specialized high endothelial venules (HEV). Exposure of splenic lymphocytes in vivo to fever-like whole-body hyperthermia (WBH; 39.8 ± 0.2°C for 6 hours) stimulated both L-selectin and α4β7 integrin–de

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Ramos, Carroll L., McRae J. Smith, Karen R. Snapp, et al. "Functional Characterization of L-Selectin Ligands on Human Neutrophils and Leukemia Cell Lines: Evidence for Mucinlike Ligand Activity Distinct From P-Selectin Glycoprotein Ligand-1." Blood 91, no. 3 (1998): 1067–75. http://dx.doi.org/10.1182/blood.v91.3.1067.

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Abstract Recent reports have shown that leukocyte-leukocyte adhesion is dependent on L-selectin and that leukocyte recognition of L-selectin may be mediated by P-selectin glycoprotein ligand-1 (PSGL-1). We show that the specific attachment and rolling of human neutrophils and the leukemia cell lines HL-60 and U937 on immobilized, purified L-selectin under continuous shear stress is only partially inhibited by treatment with the PSGL-1 monoclonal antibody (MoAb), KPL1 (41% to 53% inhibition), suggesting that L-selectin ligand activity in addition to PSGL-1 may mediate myeloid cell rolling on L-

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Ramos, Carroll L., McRae J. Smith, Karen R. Snapp, et al. "Functional Characterization of L-Selectin Ligands on Human Neutrophils and Leukemia Cell Lines: Evidence for Mucinlike Ligand Activity Distinct From P-Selectin Glycoprotein Ligand-1." Blood 91, no. 3 (1998): 1067–75. http://dx.doi.org/10.1182/blood.v91.3.1067.1067_1067_1075.

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Recent reports have shown that leukocyte-leukocyte adhesion is dependent on L-selectin and that leukocyte recognition of L-selectin may be mediated by P-selectin glycoprotein ligand-1 (PSGL-1). We show that the specific attachment and rolling of human neutrophils and the leukemia cell lines HL-60 and U937 on immobilized, purified L-selectin under continuous shear stress is only partially inhibited by treatment with the PSGL-1 monoclonal antibody (MoAb), KPL1 (41% to 53% inhibition), suggesting that L-selectin ligand activity in addition to PSGL-1 may mediate myeloid cell rolling on L-selectin.

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Zöllner, Olaf, Martin C. Lenter, James E. Blanks, et al. "L-Selectin from Human, but Not from Mouse Neutrophils Binds Directly to E-Selectin." Journal of Cell Biology 136, no. 3 (1997): 707–16. http://dx.doi.org/10.1083/jcb.136.3.707.

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L-Selectin on neutrophils as well as inducible E- and P-selectin on endothelium are involved in the recruitment of neutrophils into inflamed tissue. Based on cell attachment assays, L-selectin was suggested to function as a carbohydrate presenting ligand for E- and P-selectin. However, previous affinity isolation experiments with an E-selectin–Ig fusion protein had failed to detect L-selectin among the isolated E-selectin ligands from mouse neutrophils. We show here that L-selectin from human neutrophils, in contrast to mouse neutrophils, can be affinity-isolated as a major ligand from total c

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Shimada, Yuka, Shinichi Sato, Minoru Hasegawa, Thomas F. Tedder, and Kazuhiko Takehara. "Elevated serum L-selectin levels and abnormal regulation of L-selectin expression on leukocytes in atopic dermatitis: Soluble L-selectin levels indicate disease severity☆☆☆★." Journal of Allergy and Clinical Immunology 104, no. 1 (1999): 163–68. http://dx.doi.org/10.1016/s0091-6749(99)70128-4.

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