PSGL-1 derived from human neutrophils is a high-efficiency ligand for endothelium-expressed E-selectin under flow

Zou, Xiaoyan; Patil, Vivek R. Shinde; Dagia, Nilesh M.; Smith, Lee A.; Wargo, Maureen J.; Interliggi, Kimberly A.; Lloyd, Christopher M; Tees, David F. J.; Walcheck, Bruce; Lawrence, Michael B.; Goetz, Douglas J.

doi:10.1152/ajpcell.00289.2004

Cited by 43 publications

(57 citation statements)

References 50 publications

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“…It is interesting to note that we observed significantly higher levels of CCL2 in kidney tissue collected from 16-and 20-wk-old PSGL-1/Fas lpr mice compared with controls, while CCL2 expression was only increased in 20-wk-old samples taken from P-sel/Fas lpr mice. PSGL-1 also interacts with E-selectin on endothelial cells, and it is possible that the combined loss of PSGL-1 interactions with both of these endothelial selectins is responsible for the increase in CCL2 expression (58,59). Support for this model comes from preliminary studies in our laboratory where we have observed that E-selectin mutant Fas lpr mice also show accelerated lethality associated with the rapid development of glomerulonephritis, and increased CCL2 expression in LPS-stimulated E-selectin-deficient primary endothelial cells (X.…”

Section: Discussionmentioning

confidence: 99%

Deficiency of P-Selectin or P-Selectin Glycoprotein Ligand-1 Leads to Accelerated Development of Glomerulonephritis and Increased Expression of CC Chemokine Ligand 2 in Lupus-Prone Mice

He¹,

Schoeb²,

Panoskaltsis‐Mortari

et al. 2006

The Journal of Immunology

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The selectins and their ligands mediate leukocyte rolling on endothelial cells, the initial step in the emigration cascade leading to leukocyte infiltration of tissue. These adhesion molecules have been shown to be key promoters of acute leukocyte emigration events; however, their roles in the development of long-term inflammatory responses, including those that occur during chronic inflammatory diseases such as systemic lupus erythematosus, are unclear. To assess participation of P-selectin in such disorders, we studied the progression of systemic lupus erythematosus-like disease in P-selectin-deficient and control MRL/MpJ-Faslpr (Faslpr) mice. Surprisingly, we found that P-selectin deficiency resulted in significantly earlier mortality, characterized by a more rapid development of glomerulonephritis and dermatitis. Expression of CCL2 (MCP-1) was increased in the kidneys of P-selectin mutant mice and in supernatants of LPS-stimulated primary renal endothelial cell cultures from these mice. A closely similar phenotype, including elevated renal expression of CCL2, was also observed in Faslpr mice deficient in the major P-selectin ligand, P-selectin glycoprotein ligand-1. These results indicate that P-selectin and P-selectin glycoprotein ligand-1 are not required for leukocyte infiltration and the development of autoimmune disease in Faslpr mice, but rather expression of these adhesion molecules is important for modulating the progression of glomerulonephritis, possibly through down-regulation of endothelial CCL2 expression.

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Section: Discussionmentioning

confidence: 99%

Deficiency of P-Selectin or P-Selectin Glycoprotein Ligand-1 Leads to Accelerated Development of Glomerulonephritis and Increased Expression of CC Chemokine Ligand 2 in Lupus-Prone Mice

He¹,

Schoeb²,

Panoskaltsis‐Mortari

et al. 2006

The Journal of Immunology

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“…3A). MCAM, Ninjurin-1, and CD62E, previously shown to be involved in the recruitment of specific immune cell types to the CNS (14,15,20,35,36), were also assessed and showed no significant differences between ALCAM KO and WT mouse BBB-ECs (MBECs) either in resting or stimulated conditions (Fig. S3).…”

Section: Cd11cmentioning

confidence: 98%

Dual role of ALCAM in neuroinflammation and blood–brain barrier homeostasis

Lécuyer

Saint-Laurent

Bourbonnière

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Activated leukocyte cell adhesion molecule (ALCAM) is a cell adhesion molecule found on blood-brain barrier endothelial cells (BBB-ECs) that was previously shown to be involved in leukocyte transmigration across the endothelium. In the present study, we found that ALCAM knockout (KO) mice developed a more severe myelin oligodendrocyte glycoprotein (MOG) 35-55 -induced experimental autoimmune encephalomyelitis (EAE). The exacerbated disease was associated with a significant increase in the number of CNS-infiltrating proinflammatory leukocytes compared with WT controls. Passive EAE transfer experiments suggested that the pathophysiology observed in active EAE was linked to the absence of ALCAM on BBB-ECs. In addition, phenotypic characterization of unimmunized ALCAM KO mice revealed a reduced expression of BBB junctional proteins. Further in vivo, in vitro, and molecular analysis confirmed that ALCAM is associated with tight junction molecule assembly at the BBB, explaining the increased permeability of CNS blood vessels in ALCAM KO animals. Collectively, our data point to a biologically important function of ALCAM in maintaining BBB integrity. multiple sclerosis | ALCAM | blood-brain barrier | EAE | tight junctions

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“…The vessel wall is modeled by either coating of biomolecules or growth of cells on one surface of the flow chamber 3 . Particles [4][5][6][7] or cells [8][9][10][11][12][13][14][15][16] are then flowed in at desired range of flow rates to quantify the number of adhering particles under various shear rates.…”

Section: Introductionmentioning

confidence: 99%

Generation of Shear Adhesion Map Using SynVivo Synthetic Microvascular Networks

Prabhakarpandian

Pant

2014

JoVE

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Cell/particle adhesion assays are critical to understanding the biochemical interactions involved in disease pathophysiology and have important applications in the quest for the development of novel therapeutics. Assays using static conditions fail to capture the dependence of adhesion on shear, limiting their correlation with in vivo environment. Parallel plate flow chambers that quantify adhesion under physiological fluid flow need multiple experiments for the generation of a shear adhesion map. In addition, they do not represent the in vivo scale and morphology and require large volumes (~ml) of reagents for experiments. In this study, we demonstrate the generation of shear adhesion map from a single experiment using a microvascular network based microfluidic device, SynVivo-SMN. This device recreates the complex in vivo vasculature including geometric scale, morphological elements, flow features and cellular interactions in an in vitro format, thereby providing a biologically realistic environment for basic and applied research in cellular behavior, drug delivery, and drug discovery. The assay was demonstrated by studying the interaction of the 2 µm biotin-coated particles with avidin-coated surfaces of the microchip. The entire range of shear observed in the microvasculature is obtained in a single assay enabling adhesion vs. shear map for the particles under physiological conditions. Video LinkThe video component of this article can be found at

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PSGL-1 derived from human neutrophils is a high-efficiency ligand for endothelium-expressed E-selectin under flow

Cited by 43 publications

References 50 publications

Deficiency of P-Selectin or P-Selectin Glycoprotein Ligand-1 Leads to Accelerated Development of Glomerulonephritis and Increased Expression of CC Chemokine Ligand 2 in Lupus-Prone Mice

Deficiency of P-Selectin or P-Selectin Glycoprotein Ligand-1 Leads to Accelerated Development of Glomerulonephritis and Increased Expression of CC Chemokine Ligand 2 in Lupus-Prone Mice

Dual role of ALCAM in neuroinflammation and blood–brain barrier homeostasis

Generation of Shear Adhesion Map Using SynVivo Synthetic Microvascular Networks

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