β2-glycoprotein-I (apo-H) inhibits the release reaction of human platelets during ADP-induced aggregation

Nimpf, Johannes; Wurm, H.; Kostner, Gerhard M.

doi:10.1016/0021-9150(87)90110-9

Cited by 194 publications

(76 citation statements)

References 18 publications

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“…This cofactor was identified as 2 -GPI (also called apolipoprotein H) [6]. Various physiological functions of 2 -GPI have been reported: inhibition of the intrinsic coagulation pathway [7], of adenosine diphosphate (ADP)-mediated platelet aggregation [8], and of prothrombinase activity of activated platelets [9].…”

Section: Introductionmentioning

confidence: 99%

Measurement of anticardiolipin antibodies by ELISA using β2-glycoprotein I (β2-GPI) in systemic sclerosis

Ihn

Sato

Fujimoto

et al. 1996

Clinical and Experimental Immunology

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SUMMARYIn order to determine the prevalence and clinical significance of¯2-GPI-dependent anticardiolipin antibodies (¯2-GPI/aCL) in patients with systemic sclerosis (SSc), serum samples from 80 patients with SSc, 20 patients with systemic lupus erythematosus (SLE), and 120 healthy control subjects were examined by ELISA using purified¯2-GPI. IgG isotype¯2-GPI/aCL was present in eight of 80 patients with SSc (10%), and the presence of¯2-GPI/aCL IgG was significantly correlated with the presence of isolated pulmonary hypertension (PH). Furthermore, levels of¯2-GPI/aCL IgG were significantly correlated with levels of mean pulmonary arterial pressure. These data suggest that IgG isotype¯2-GPI/ aCL might be a serological indicator of the severity of PH in patients with SSc.

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Section: Introductionmentioning

confidence: 99%

Measurement of anticardiolipin antibodies by ELISA using β2-glycoprotein I (β2-GPI) in systemic sclerosis

Ihn

Sato

Fujimoto

et al. 1996

Clinical and Experimental Immunology

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“…Beta,-glycoprotein I is a cationic protein that is able to play a natural anticoagulant role by binding to anionic procoagulant surfaces, including membranes of cells involved in the coagulation cascade (23)(24)(25)(26). In view of this, &GPI binding to human EC membranes has recently been reported in both in vitro and ex vivo studies (27)(28)(29).…”

mentioning

confidence: 99%

Endothelial cells as target for antiphospholipid antibodies. Human Polyclonal and Monoclonal Anti‐β₂‐Glycoprotein I Antibodies React In Vitro with Endothelial Cells Through Adherent β₂‐Glycoprotein I and Induce Endothelial Activation

Papa

Guidali

Sala

et al. 1997

Arthritis & Rheumatism

270

142

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Objective. To investigate the ability of human anti-&-glycoprotein I (anti-&GPI) antibodies to recognize the cofactor adherent on endothelial cells (EC) and to modulate endothelial functions.Methods. Six human affinity-purified polyclonal anti-P,GPI IgG and 2 IgM monoclonal antibodies (MAb) were obtained from patients with the antiphospholipid syndrome. The antibodies were tested for their ability to 1) bind to endothelial monolayers through the adherent f3,GPI and 2) modulate endothelial adhesion molecule expression and interleukin-6 (IL-6) and 6-keto-prostaglandin F,, (6-keto-PGF1,) secretion.Results. The affinity-purified IgG and the MAb with anti-&GPI activity, but not the respective controls, displayed EC binding, which declined on cells incubated in serum-free medium and was restored in a dose-dependent manner by exogenous human P,GPI. After EC binding, both polycJonaJ and monoclonal antibodies up-regulated adhesion molecule expres-

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“…The fifth sushi-domain contains the binding site to phospholipid, and it attaches to activated cellular surfaces [31]. β2-GPI binds to various negatively charged phospholipids and inhibits intrinsic blood coagulation pathway [32], prothrombinase activity of human platelets [33] , and adenosine diphosphate (ADP) dependent platelet aggregation [34]. When β2-GPI binds to negatively charged phospholipids, it behaves as a cofactor for aCL binding and interacts with coagulation reactions.…”

Section: Genes Associated With Antiphospholipid Syndromementioning

confidence: 99%

Genetics of Antiphospholipid Syndrome

Hancer¹

2011

Human Genet Embryol

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Antiphospholipid syndrome (APS) is defined as recurrent arterial and/or venous thrombosis and obstetric complications in the presence of antiphospholipid antibodies (aPL). The possibility of a genetic predisposition to develop antiphospholipid syndrome (APS) and to produce anticardiolipin antibodies and lupus anticoagulant has been examined by family studies and population studies. Similar to many other polygenic autoimmune diseases, human leukocyte antigen associations have been reported. The genetics of β2-glycoprotein I, one of the most representative target antigens of aPL, has been extensively studied. Additional genetic risk factors for the development of thrombosis in patients with aPL have also been discussed. Although the mechanisms and pathophysiology of thrombosis in APS are highly heterogeneous and multifactorial, different genes seem to be involved.The term "antiphospholipid syndrome" has been proposed to describe the association of arterial and venous thrombosis, recurrent fetal loss, and immune thrombocytopenia with a spectrum of autoantibodies directed against cellular phospholipid components. Because of the antigen spesifity of antiphospholipid antibodies (aPL) and the pathophysiology of thrombosis in antiphospholipid syndrome (APS) are heterogeneous and multifactorial, a single scenario can not explain the mechanisms of thrombophilia or pregnancy morbidity in pateints. Investigation of the clinical epidemiology of APS is in its early stages. During the past 20 years, studies of aPL and APS have been made in many countries [1][2][3][4][5][6][7][8][9][10][11]. aPL appear to occur in all populations studied, with some variations noted in their frequency and in the clinical complications [1,9,10,12,13]. Environmental and genetic factors contribute to ethnic variation and susceptibility to APS and thus interethnic differences in disease patterns may be due to environmental or genetic factors, or both [1,14]. A genetic basis for aPL antibodies was suggested for the first time when a familial clustering of chronic false-positive syphilis test individuals were detected [15]. The first description about aPL showed two pairs of siblings with lupus anticoagulant (LA) [16]. Subsequently, primary APS was described [17] and Cevallos et al. [18] reported the development of primary APS in one woman whose identical twin sister was an asymptomatic carrier of aPL. Relatives of patients with sistemic lupus erythematosus (SLE) or primary APS had a higher incidence of anticardiolipin antibodies (aCL) [19,20] suggesting that a genetic factor may relevant with aPL. Mackie et al. [21] reported three families having more than one member with LA and called familial lupus anticoagulants. The identification of several pedigrees with an increased frequency of aPL antibodies and the associated clinical manifestations further support the familial form of APS. In one of these studies, a large kindred in which nine individuals had aPL antibodies was described. Associated clinical manifestations included stroke, deep ve...

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β2-glycoprotein-I (apo-H) inhibits the release reaction of human platelets during ADP-induced aggregation

Cited by 194 publications

References 18 publications

Measurement of anticardiolipin antibodies by ELISA using β2-glycoprotein I (β2-GPI) in systemic sclerosis

Measurement of anticardiolipin antibodies by ELISA using β2-glycoprotein I (β2-GPI) in systemic sclerosis

Endothelial cells as target for antiphospholipid antibodies. Human Polyclonal and Monoclonal Anti‐β₂‐Glycoprotein I Antibodies React In Vitro with Endothelial Cells Through Adherent β₂‐Glycoprotein I and Induce Endothelial Activation

Genetics of Antiphospholipid Syndrome

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β2-glycoprotein-I (apo-H) inhibits the release reaction of human platelets during ADP-induced aggregation

Cited by 194 publications

References 18 publications

Measurement of anticardiolipin antibodies by ELISA using β2-glycoprotein I (β2-GPI) in systemic sclerosis

Measurement of anticardiolipin antibodies by ELISA using β2-glycoprotein I (β2-GPI) in systemic sclerosis

Endothelial cells as target for antiphospholipid antibodies. Human Polyclonal and Monoclonal Anti‐β2‐Glycoprotein I Antibodies React In Vitro with Endothelial Cells Through Adherent β2‐Glycoprotein I and Induce Endothelial Activation

Genetics of Antiphospholipid Syndrome

Contact Info

Product

Resources

About

Endothelial cells as target for antiphospholipid antibodies. Human Polyclonal and Monoclonal Anti‐β₂‐Glycoprotein I Antibodies React In Vitro with Endothelial Cells Through Adherent β₂‐Glycoprotein I and Induce Endothelial Activation