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Platelet membrane glycoprotein complex important for platelet adhesion and aggregation. It is an integrin complex containing INTEGRIN ALPHAIIB and INTEGRIN BETA3 which recognizes the arginine-glycine-aspartic acid (RGD) sequence present on several adhesive proteins. As such, it is a receptor for FIBRINOGEN; VON WILLEBRAND FACTOR; FIBRONECTIN; VITRONECTIN; and THROMBOSPONDINS. A deficiency of GPIIb-IIIa results in GLANZMANN THROMBASTHENIA.
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Physiologically active compounds found in many organs of the body. They are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase.
Patients who have been treated with Glycoprotein IIb/IIIa inhibitors should not be tested until platelet function has recovered. This time period is approximately 14 days after discontinuation of abciximab (ReoPro) and up to 48 hours after discontinuation of eptifibatide (Integrilin) and tirofiban (Aggrastat.
Despite considerable research into pharmacologic and revascularization treatments for the acute coronary ischemic syndromes, outcome among patients hospitalized with unstable angina remains unsatisfactory. Recently reported large-scale randomized trials, for example, have demonstrated that the risk of death or MI within the first 4 to 6 weeks after development of unstable angina is as high as 9% to 11% ([27, 28]).
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N2 - We aimed to clarify the disability progression and platelet aggregative function in atopic myelitis (AM). Seventeen AM patients and 35 healthy controls were subjected to clinico-allergological evaluations and glycoprotein IIb/IIIa (GP IIb/IIIa) measurements using a VerifyNow assay system. In AM patients, the disease duration had significant positive correlations with the Kurtzke Expanded Disability Status Scale scores and Sensory Functional Scale scores. The GP IIb/IIIa values were significantly higher in AM patients than in controls as well as in females compared with males. AM is essentially a progressive disease affecting the sensory.
Platelet Glycoprotein GPIIb-IIIa Complex < Platelet Membrane Glycoproteins
D3 phosphoinositides and outside-in integrin signaling by GPIIb/IIIa mediate platelet actin assembly and filopodial extension. Localization of the domain actin-binding protein that binds to glycoprotein Ib and actin in human platelets.
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An antibiotic mixture of two components, A and B, obtained from Nocardia lurida (or the same substance produced by any other means). It is no longer used clinically because of its toxicity. It causes platelet agglutination and blood coagulation and is used to assay those functions in vitro.
An unstable intermediate between the prostaglandin endoperoxides and thromboxane B2. The compound has a bicyclic oxaneoxetane structure. It is a potent inducer of platelet aggregation and causes vasoconstriction. It is the principal component of rabbit aorta contracting substance (RCS).
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The central role played by the alphaIIb beta3 receptor in platelet aggregation, and hence in platelet thrombosis, has led to the development of a number of parenteral and oral glycoprotein (GP) IIb/IIIa inhibitors for use in cardiovascular disease states, such as acute coronary syndromes and stroke. The predominant effect of these agents is to inhibit platelet aggregation, although studies of alphaIIb beta3 receptor function and various GP IIb/IIIa inhibitors have demonstrated the potential for these agents to produce effects on other aspects of platelet function, in addition to non-platelet effects. Overall, clinical studies have demonstrated an impressive beneficial effect for parenteral agents in reducing ischemic complications following percutaneous intervention, and a more modest beneficial effect in the treatment of patients with acute coronary syndromes. Trials with oral GP IIb/IIIa inhibitors in similar patient populations have demonstrated toxicity, manifested by an increased mortality.
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A plasma protein that is the inactive precursor of thrombin. It is converted to thrombin by a prothrombin activator complex consisting of factor Xa, factor V, phospholipid, and calcium ions. Deficiency of prothrombin leads to hypoprothrombinemia.
Eptifibatide (Integrilin, Millennium Pharmaceuticals, also co-promoted by Schering-Plough/Essex), is an antiplatelet drug of the glycoprotein IIb/IIIa inhibitor class. Eptifibatide is a cyclic heptapeptide derived from a protein found in the venom of the southeastern pygmy rattlesnake (Sistrurus miliarius barbouri). It belongs to the class of the arginin-glycin-aspartat-mimetics and reversibly binds to platelets. Eptifibatide has a short half-life. The drug is the third inhibitor of GPIIb/IIIa that has found broad acceptance after the specific antibody abciximab and the non-peptide tirofiban entered the global market. Integrilin is sold in two strengths, globally: vials containing 2 mg/ml (20 mg totally) and 0/75 mg/ml (75 mg totally). A third size is sold in the US: 100 ml vials containing 2 mg/ml (200 mg totally).
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The largest class of organic compounds, including STARCH; GLYCOGEN; CELLULOSE; POLYSACCHARIDES; and simple MONOSACCHARIDES. Carbohydrates are composed of carbon, hydrogen, and oxygen in a ratio of Cn(H2O)n.
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The sensitivity for coagulation factor. Moreover, it is successfully used in the complex situation of (poly)trauma, or in decision making for of alternative therapy. FIBTEM eliminates the platelet contribution of clot formation by inhibiting the platelets irreversibly with cytochalasin D, a.
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
Glycoproteins found on the surfaces of cells, particularly in fibrillar structures. The proteins are lost or reduced when these cells undergo viral or chemical transformation. They are highly susceptible to proteolysis and are substrates for activated blood coagulation factor VIII. The forms present in plasma are called cold-insoluble globulins.
Layers of protein which surround the capsid in animal viruses with tubular nucleocapsids. The envelope consists of an inner layer of lipids and virus specified proteins also called membrane or matrix proteins. The outer layer consists of one or more types of morphological subunits called peplomers which project from the viral envelope; this layer always consists of glycoproteins.
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Abciximab (ReoPro®) is the oldest and it produces note that the complications were even more frequent in an almost irreversible inhibition of the GP IIa/IIIb recep- patients using NSAIDs with a half-life of ,6 hours (Figure 2). tors. Two more recent products, eptifibatide (Integrelin®) In a series of 1000 orthopedic surgeries performed on and tirofiban (Aggrastat®), produce a comparable inhibi- 924 patients, there were no reports of perimedullar tion of the GP IIb/IIIa receptors. All are rapid-acting with hematoma with either spinal or epidural anesthesia.
The binding of low density lipoprotein (LDL) to the platelet cell membrane could facilitate the transfer of phospholipids from LDL to the platelets. A polyclonal antibody against the platelet glycoproteins IIb/IIIa inhibited the high affinity binding of 125I-LDL by up to 80%. The transfer of pyrene (py)-labeled sphingomyelin (SM), phosphatidylcholine and phosphatidylethanolamine from LDL to the platelets was unaffected by the antibody. The lectin wheat germ agglutinin (WGA) reduced the binding of 125I-LDL to the platelets by approximately 80%. In contrast, the lectin stimulated the transfer of SM from LDL into the platelets by about three-fold. WGA also specifically augmented the transfer of py-SM between lipid vesicles and the platelets, the stimulation being abolished in the presence of N-acetylglucosamine. Dextran sulfate (DS) increased the specific binding of 125I-LDL to the platelets by up to 2/8-fold. On the other hand, the import of LDL-derived py-phospholipids was unaffected by DS. Together, the results indicate that the phospholipid transfer from LDL to the platelets is independent of the high affinity LDL binding to the platelets and is specifically stimulated by WGA.
Any of various enzymatically catalyzed post-translational modifications of PEPTIDES or PROTEINS in the cell of origin. These modifications include carboxylation; HYDROXYLATION; ACETYLATION; PHOSPHORYLATION; METHYLATION; GLYCOSYLATION; ubiquitination; oxidation; proteolysis; and crosslinking and result in changes in molecular weight and electrophoretic motility.
An integrin alpha subunit that primarily combines with INTEGRIN BETA1 to form the INTEGRIN ALPHA2BETA1 heterodimer. It contains a domain which has homology to collagen-binding domains found in von Willebrand factor.
Proteins which contain carbohydrate groups attached covalently to the polypeptide chain. The protein moiety is the predominant group with the carbohydrate making up only a small percentage of the total weight.
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A genus of the subfamily CERCOPITHECINAE, family CERCOPITHECIDAE, consisting of five named species: PAPIO URSINUS (chacma baboon), PAPIO CYNOCEPHALUS (yellow baboon), PAPIO PAPIO (western baboon), PAPIO ANUBIS (or olive baboon), and PAPIO HAMADRYAS (hamadryas baboon). Members of the Papio genus inhabit open woodland, savannahs, grassland, and rocky hill country. Some authors consider MANDRILLUS a subgenus of Papio.
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All enrolled patients would be followed-up to 30 days, 6 months, and 1 year. The purpose of the study is to evaluate the efficacy and safety of bivalirudin in AMI patients with DES.
A product of the lysis of plasminogen (profibrinolysin) by PLASMINOGEN activators. It is composed of two polypeptide chains, light (B) and heavy (A), with a molecular weight of 75,000. It is the major proteolytic enzyme involved in blood clot retraction or the lysis of fibrin and quickly inactivated by antiplasmins.
Glycoprotein IIb/IIIa inhibitors are established treatment for Patients who develop acute coronary syndromes. Thrombocytopenia is known to occur following the administration of various drugs, including heparin and glycoprotein IIb/IIIa inhibitors, In the case of glycoprotein IIb/IIIa inhibitors, the mechanism is thought to be drug-dependent antibodies. In most cases, the thrombocytopenia is mild or moderate in severity.
An adhesion-promoting leukocyte surface membrane heterodimer. The alpha subunit consists of the CD11b ANTIGEN and the beta subunit the CD18 ANTIGEN. The antigen, which is an integrin, functions both as a receptor for complement 3 and in cell-cell and cell-substrate adhesive interactions.
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Amidines substituted with a benzene group. Benzamidine and its derivatives are known as peptidase inhibitors.
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A superiority for the anti-clotting drug bivalirudin for treating patients with acute coronary syndromes was detected when this was used as monotherapy, but not when this direct thrombin inhibitor was combined with glycoprotein IIb/IIIa inhibition. Thus found the ACUITY trial reported to the ACCs Atlanta meeting by Gregg Stone of Columbia University. He told Audio Medica the bottom line finding from the study.
The process of generating thrombocytes (BLOOD PLATELETS) from the pluripotent HEMATOPOIETIC STEM CELLS in the BONE MARROW via the MEGAKARYOCYTES. The humoral factor with thrombopoiesis-stimulating activity is designated THROMBOPOIETIN.
Univalent antigen-binding fragments composed of one entire IMMUNOGLOBULIN LIGHT CHAIN and the amino terminal end of one of the IMMUNOGLOBULIN HEAVY CHAINS from the hinge region, linked to each other by disulfide bonds. Fab contains the IMMUNOGLOBULIN VARIABLE REGIONS, which are part of the antigen-binding site, and the first IMMUNOGLOBULIN CONSTANT REGIONS. This fragment can be obtained by digestion of immunoglobulins with the proteolytic enzyme PAPAIN.
The limited current understanding of megakaryocyte-lineage development and megakaryocyte biology is in large part because of a paucity of useful systems in which to conduct experiments. To overcome this problem, we have developed a transgenic mouse that uses the GP-Ibalpha regulatory sequences to achieve megakaryocyte-lineage restricted expression of an avian retroviral receptor. Through the transgenic avian receptor, avian retroviruses can efficiently and selectively infect megakaryocyte-lineage cells in vitro and in vivo. Serial infections can be performed to introduce and express multiple genes in the same cell.
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Cell surface proteins that bind signalling molecules external to the cell with high affinity and convert this extracellular event into one or more intracellular signals that alter the behavior of the target cell (From Alberts, Molecular Biology of the Cell, 2nd ed, pp693-5). Cell surface receptors, unlike enzymes, do not chemically alter their ligands.
In animals it is synthesized from PHENYLALANINE. It is also the precursor of EPINEPHRINE; THYROID HORMONES; and melanin.
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A calcium-activated enzyme that catalyzes the hydrolysis of ATP to yield AMP and orthophosphate. It can also act on ADP and other nucleoside triphosphates and diphosphates.
Thrombocytopenia occurring in the absence of toxic exposure or a disease associated with decreased platelets. It is mediated by immune mechanisms, in most cases IMMUNOGLOBULIN G autoantibodies which attach to platelets and subsequently undergo destruction by macrophages. The disease is seen in acute (affecting children) and chronic (adult) forms.
The identification of stromal cell-derived factor (SDF)-1alpha as a chemoattractant for human progenitor cells suggests that this chemokine and its receptor might represent critical determinants for the homing, retention, and exit of precursor cells from hematopoietic organs. In this study, we investigated the expression profile of CXCR4 receptor and the biological activity of SDF-1alpha during megakaryocytopoiesis. CD34(+) cells from bone marrow and cord blood were purified and induced to differentiate toward the megakaryocyte lineage by a combination of stem-cell factor (SCF) and recombinant human pegylated megakaryocyte growth and development factor (PEG-rhuMGDF). After 6 days of culture, a time where mature and immature megakaryocytes were present, CD41(+) cells were immunopurified and CXCR4mRNA expression was studied. High transcript levels were detected by a RNase protection assay in cultured megakaryocytes derived from cord blood CD34(+) cells as well as in peripheral blood platelets. The transcript levels were about equivalent to that found in activated T cells. By flow cytometry, a large fraction (ranging from 30% to 100%) of CD41(+) cells showed high levels of CXCR4 antigen on their surface, its expression increasing in parallel with the CD41 antigen during megakaryocytic differentiation. CXCR4 protein was also detected on peripheral blood platelets. SDF-1alpha acts on megakaryocytes by inducing intracellular calcium mobilization and actin polymerization. In addition, in in vitro transmigration experiments, a significant proportion of megakaryocytes was observed to respond to this chemokine.
Fibrin participates in limiting blood. Fibrinogen (factor I) is a glycoprotein complex, made in the liver, that circulates in the blood of all vertebrates.
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When bivalirudin was compared with unfractionated heparin alone there was no benefit in ischemic complications with a decrease in major bleeding. However, in a recent large randomized controlled trial comparing bivalirudin with unfractionated heparin alone in AMI patients undergoing primary PCI, bivalirudin did not.
This study sought to determine whether depressive symptoms and/or platelet serotonin receptor (5HT2A) density are associated with increased platelet activation (PA) found among smokers. Flow cytometric detection of PA was used to study 36 smokers and 16 nonsmokers, aged 18 to 48 years. Subjects were tested at baseline and after either smoking 2 cigarettes (smokers) or a similar resting interval (nonsmokers). Assessment of PA included both platelet secretion and fibrinogen receptor (GPIIb/IIIa) binding. Platelet 5HT2A receptor binding and saturation were tested using [3H]LSD, and depressive symptoms were measured using the Beck Depression Inventory.
Keywords: platelet, IIIa antagonist, abciximab, eptifibatide, tirofiban, lamifiban, thrombocytopenia, angioplasty. Abstract: The activation of platelets and the resultant aggregation have been shown to play important role in the pathogenesis of cardiovascular, cerebrovascular and peripheral vascular diseases and in acute coronary syndromes. Hence platelet adhesion and aggregation have been identified as promising targets for the development of anti-thrombotic drugs. Glycoprotein (GP) IIb / IIIa antagonism exerts a strong anti-platelet effect, because this interference inhibits the final common pathway of platelet aggregation and is not dependent on a single activation pathway. Three GPIIb / IIIa antagonists have been approved by the US Food and Drug administration. They include abciximab (the chimeric monoclonal antibody 7E3 Fab fragment), eptifibatide (the cyclic heptapeptide based on the KGD amino acid sequence) and tirofiban (a nonpeptide tyrosine derivative).
Abciximab is a new antiplatelet therapeutic in ischemic cardiovascular disease. The drug, chimeric Fab fragments of a murine monoclonal antibody (MoAb) (c7E3), blocks GP IIb-IIIa function. However, its capacity to reach all receptor pools in platelets is unknown. Electron microscopy and immunogold labeling were used to localize abciximab in platelets of patients receiving the drug for up to 24 hours. Studies on frozen-thin sections showed that c7E3 Fab, in addition to the surface pool, also labeled the surface-connected canalicular system (SCCS) and alpha-granules. Analysis of gold particle distribution showed that intraplatelet labeling was not accumulative and in equilibrium with the surface pool. After short-term incubations of platelets with c7E3 Fab in vitro, gold particles were often seen in lines within thin elements of the SCCS, some of which appeared in contact with alpha-granules. Little labeling was associated with Glanzmann's thrombasthenia platelets, confirming that the channels contained bound and not free c7E3 Fab. Endocytosis of abciximab in clathrin-containing vesicles was visualized by double staining and constitutes an alternative mechanism of transport. The remaining free pool of GP IIb-IIIa was evaluated with the MoAb AP-2; flow cytometry showed it to be about 9% on the surface of nonstimulated platelets but 33% on thrombin-activated platelets.
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For example, GPIb/IX/V; GPVI; GPIIb/IIIa. An overview summarizing platelet dynamics, the complex process of converting inactive platelets into a platelet plug, is. activated platelets with exposed GPIIb/IIIa can bind fibrinogen to aggregate. GPIIb/IIIa may also further anchor the platelets. Platelets also secrete platelet-derived growth factor (PDGF). Platelets modulate neutrophils by forming platelet-leukocyte.
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The ability of high shear to activate platelets and induce their adhesion and aggregation has been well studied (Ruggeri, 1993; Kroll et al, 1996; Frojmovic, 1998). The importance of shear in platelet adhesion and aggregation has been viewed in the perspective of arterial stenosis caused by atherosclerotic plaques in the coronary, carotid, and peripheral arteries. The interaction of vWF with the glycoprotein Ib/IX/V complex is the initial step that is followed by the binding of vWF to glycoprotein IIb/IIIa to induce platelet activation and aggregation (Kroll et al, 1996). Shear-induced platelet aggregation is often associated with platelet thrombus formation (Kroll et al, 1996). The exposed subendothelium in pathological conditions can serve as the substrate for platelet adhesion and aggregation under elevated shear stress. Such shear-induced platelet-surface interaction is known to be mediated between the functional glycoprotein IIb/IIIa receptors and collagen, vWF, fibrin(ogen).
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The influence of antiplatelet glycoprotein (GP) antibodies on megakaryocytopoiesis in patients with idiopathic or immune thrombocytopenic purpura (ITP) has been well studied. However, the influence of GP antibodies on proplatelet formation is poorly understood. Here we investigated whether in vitro human megakaryocyte colony formation and proplatelet formation are affected by various monoclonal antiplatelet GP antibodies (MoAb). The megakaryocyte colony formation inhibition assay was performed by methylcellulose culture with modifications, using peripheral blood nonadherent mononuclear cells. The proplatelet formation inhibition assay was performed by megakaryocytes derived from CD34(+) cells, stimulated with thrombopoietin + stem cell factor, which were then incubated with antiplatelet GP MoAb for 24 or 48 hours.
Platelet aggregation is achieved by mediating expression of the glycoprotein complex GP IIb/IIIa in the cell membrane of. Thromboxane A2 (TXA2), produced by activated platelets, has prothrombotic properties, stimulating activation of new platelets. If the cap of a vulnerable plaque erodes or ruptures, as in myocardial infarction, platelets stick to the damaged lining of the. The mechanism of secretion of thromboxanes from platelets is still unclear. They act in the formation of blood clots and reduce.