Platelet glycocalicin. II. Purification and characterization.

Okumura, Itsuo; Lombart, Christian; Jamieson, G.A.

doi:10.1016/s0021-9258(17)33044-2

Cited by 141 publications

(12 citation statements)

References 16 publications

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“…The highly glycosylated GPIb-IX-V complex plays an important role in platelet clearance, as the majority of desialylation occurs on GPIbα [ 281 ]. The clustering of GPIbα not only mediates platelet aggregation but also clearance.…”

Section: Monocytesmentioning

confidence: 99%

Beyond Hemostasis: Platelet Innate Immune Interactions and Thromboinflammation

Mandel

Casari

Stepanyan

et al. 2022

IJMS

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There is accumulating evidence that platelets play roles beyond their traditional functions in thrombosis and hemostasis, e.g., in inflammatory processes, infection and cancer, and that they interact, stimulate and regulate cells of the innate immune system such as neutrophils, monocytes and macrophages. In this review, we will focus on platelet activation in hemostatic and inflammatory processes, as well as platelet interactions with neutrophils and monocytes/macrophages. We take a closer look at the contributions of major platelet receptors GPIb, αIIbβ3, TLT-1, CLEC-2 and Toll-like receptors (TLRs) as well as secretions from platelet granules on platelet–neutrophil aggregate and neutrophil extracellular trap (NET) formation in atherosclerosis, transfusion-related acute lung injury (TRALI) and COVID-19. Further, we will address platelet–monocyte and macrophage interactions during cancer metastasis, infection, sepsis and platelet clearance.

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Section: Monocytesmentioning

confidence: 99%

Beyond Hemostasis: Platelet Innate Immune Interactions and Thromboinflammation

Mandel

Casari

Stepanyan

et al. 2022

IJMS

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“…9 The amino-terminus globular domain of the a subunit HE RARE CONGENITAL disorder of platelets initially described by Bernard and Soulier in 1948 1 and inherited in an autosomal recessive manner is characterized by a contains the binding site for vWF. 10 The external portion of the a chain, termed glycocalicin (135 kD), 11 can be cleaved decreased number of large, morphologically abnormal platelets and a prolonged cutaneous bleeding time. 2 Bernard-Sou-from the platelet surface and found in circulation in normal plasma.…”

mentioning

confidence: 99%

A Dinucleotide Deletion Results in Defective Membrane Anchoring and Circulating Soluble Glycoprotein Ibα in a Novel Form of Bernard-Soulier Syndrome

Kenny

Newman²,

Morateck³

et al. 1997

Blood

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The platelet membrane glycoprotein (GP)Ib-V-IX complex is the receptor for von Willebrand factor and is composed of four membrane-spanning polypeptides: GPIbα, GPIbβ, GPIX, and GPV. A qualitative or quantitative deficiency in the GPIb-V-IX complex on the platelet membrane is the cause of the congenital platelet disorder Bernard-Soulier syndrome (BSS). We describe the molecular basis of a novel variant BSS in a patient in which GPIbα was absent from the platelet surface but present in a soluble form in the plasma. DNA sequence analysis showed a homozygous dinucleotide deletion in the codon for Tyr 508 (TAT) in GPIbα. This mutation (GPIbαΔAT) causes a frame shift that alters the amino acid sequence of GPIbα within its transmembrane region. The hydrophobic nature of the predicted transmembrane region and the cytoplasmic tail at the COOH terminal are altered before reaching a new premature stop codon 38 amino acids short of the wild-type peptide. Although GPIbαΔAT was not detectable on the platelet surface, immunoprecipitation of plasma with specific monoclonal antibodies (MoAbs) identified circulating GPIbα. Transient expression of recombinant GPIbαΔAT in 293T cells also generated a soluble form of the protein. Moreover, when a plasmid encoding GPIbαΔAT was transiently transfected into Chinese hamster ovary (CHO) cells stably expressing the GPβ-IX complex, it failed to be expressed on the cell surface. Thus, a dinucleotide deletion in the codon for Tyr 508 causes a frameshift that alters the amino acid sequence of GPIbα starting within its transmembrane region, changes the hydrophobicity of the normal transmembrane region, and truncates the cytoplasmic domain affecting binding to the cytoskeleton and cytoplasmic proteins. This mutation affects anchoring of the GPIbα polypeptide in platelets and causes the observed BSS phenotype with circulating soluble GPIbα.

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“…In contrast, only one peak of radioactivity was ever observed after SDS/polyacrylamide-gel electrophoresis of the soluble fraction of surface-labelled platelets. The polypeptide in the soluble fraction is most probably glycocalicin, a surface-membrane glycoprotein previously shown to be released on sonication of platelets (Okumura et al, 1976;Nachman et al, 1979). Release of multiple copies of a specific surface glycoprotein on cell disruption is not a particular feature of platelets, since the major surface antigen of the biologically dissimilar cells of Trypanosoma brucei is also released into soluble form on cell rupture (Cross, 1975).…”

Section: Discussionmentioning

confidence: 95%

Interactions between platelet-surface glycoproteins. Identification of glycoproteins capable of binding to platelet surfaces

Bowles¹,

Brunton²

1982

Biochemical Journal

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1. Platelets have been isolated from plasma and their surface glycoconjugates radioactively-labelled using galactose oxidase and NaB3H4. 2. Conditions have been defined for optimal labelling of glycoproteins and a membrane fraction enriched in plasma membrane has been prepared and characterized by sodium dodecyl sulphate/polyacrylamide-gel electrophoresis. 3. Desialylated glycoproteins that act as receptors to peanut agglutinin and lentil lectin have been purified from a detergent extract of plasma membrane. 4. Two glycosylated polypeptides that are able to bind to the surfaces of platelets have been identified and some characteristics of the binding have been investigated.

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Platelet glycocalicin. II. Purification and characterization.

Cited by 141 publications

References 16 publications

Beyond Hemostasis: Platelet Innate Immune Interactions and Thromboinflammation

Beyond Hemostasis: Platelet Innate Immune Interactions and Thromboinflammation

A Dinucleotide Deletion Results in Defective Membrane Anchoring and Circulating Soluble Glycoprotein Ibα in a Novel Form of Bernard-Soulier Syndrome

Interactions between platelet-surface glycoproteins. Identification of glycoproteins capable of binding to platelet surfaces

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