Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02749 (beta2-glycoprotein I)
 836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Apolipoprotein H (apo H), also known as beta2-glycoprotein 1, has recently become of interest in the field of haemostasis. As apo H is elevated in diabetes mellitus and dyslipidaemia, we wished to test the hypothesis that serum apo H concentration was related to fasting plasma glucose and insulin as well as blood pressure, body mass index, hip/waist ratio and serum lipids in normal individuals. Eighty-one healthy young individuals (46 females and 35 males) were studied. Their age was 20.7 +/- 0.75 years. Serum apo H significantly correlated with fasting plasma glucose (r = 0.24, P = 0.03) and serum LDL cholesterol (r = 0.30, P = 0.006). In the females serum apo H significantly correlated with serum cholesterol concentration (r = 0.30, P = 0.04) and in males with serum HDL cholesterol concentration (r = 0.35, P = 0.04). In multifactorial regression analysis for serum apo H and the other variables for the 81 subjects, only gender and fasting plasma glucose remained statistically significant in the model. Serum apo H concentrations would be expected to increase by 21.7 mg/L for each single mmol/L increase in fasting plasma glucose (95% CI 2.3-41 2), P = 0.029, and to increase by 17.0 mg/L if the gender is male (95% Cl 0.7-332), P= 0.041.
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PMID:Serum apolipoprotein H and its relationship to blood pressure, serum lipids, fasting plasma glucose and insulin in normal individuals. 1158 27

The antiphospholipid syndrome (APS) is a disorder of hypercoagulability, characterised by thromboembolic events, repeated miscarriages and thrombocytopenia in association with circulating antiphospholipid antibodies. These antibodies are directed against epitopes on either oxidised phospholipids complexed with a glycoprotein, beta 2-glycoprotein I, or against the glycoprotein itself. Renal manifestations of the APS are varied and depend on the type of renal pathology present. The renal vasculature may be affected by either a small vessel, thrombotic microangiopathy process or by large vessel thrombosis. In patients with end stage renal disease, the prevalence of antiphospholipid antibodies may increase with time on dialysis. Anticardiolipin antibodies have been associated with a high incidence of haemodialysis access clotting, a major source of morbidity and hospitalisation in end stage renal disease patients. In renal transplant recipients, antiphospholipid antibodies may be associated with a higher incidence of primary graft non-function, particularly in patients without a history of pretransplantation haemodialysis. Complications of the APS during pregnancy span all trimesters and include intrauterine growth retardation, placental abruption, pre-eclampsia, preterm labour and recurrent fetal loss. As these women have a high risk of recurrent fetal loss, multiple treatment modalities have been investigated, including aspirin, heparin, prednisone and intravenous immunoglobulin. Various treatment strategies for the APS have been developed and are based on a combination of anticoagulant therapy with either warfarin or heparin, along with antiplatelet therapy with aspirin. Experimental treatments involving immunomodulatory therapy with intravenous immunoglobulin, apheresis and novel antibody therapy are being investigated with hopes of successful clinical applications.
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PMID:Nephrological and obstetric complications of the antiphospholipid syndrome. 1203 25

The association of antiphospholipid antibodies (APA) has been reported in several cases of patients with non-Hodgkin's lymphoma (NHL) with or without thromboembolic complications. The purpose of this study was to analyse systematically the prevalence of APA and its clinical significance in lymphoma patients. Sera of 90 consecutive unselected patients with NHL were tested for the presence of anticardiolipin (aCL) antibodies and anti-beta2-glycoprotein-I (anti-beta2-GPI) antibodies. The patients were followed up over a median period of 14 months to note the occurrence of thromboembolism. We found APA in 24 out of 90 NHL patients (26.6%). Elevated APA were more often detected in women and in the elderly. The presence of elevated APA was not correlated with the histology and the stage of the lymphoma. None of the 24 patients with elevated APA developed a thromboembolic event in the follow-up period. Thromboembolic events were observed in 12 patients (13.3%), all with negative APA. High APA titres and the combination of positive aCL- and anti-beta2-GPI antibodies, features which are known to be more strongly correlated with thrombosis among patients with antiphospholipid syndrome and systemic lupus erythematous (SLE), were very uncommon in our cohort of NHL patients (3.3%). Vessel compression by lymphoma but not elevated APA remains the main cause of thrombosis in NHL patients.
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PMID:Prevalence and clinical significance of anticardiolipin and anti-beta2-glycoprotein-I antibodies in patients with non-Hodgkin's lymphoma. 1203 53

Apolipoprotein H (ApoH), also known as beta(2)-glycoprotein I, is a plasma glycoprotein with its in vivo physiological and pathogenic roles being closely related to its interaction with negatively charged membranes. Although the three-dimensional crystal structure of ApoH has been recently solved, direct evidence about the spatial state of ApoH on the membrane is still lacking. In this work, the interactions of ApoH with the lipid layer are studied by a combination of lipid monolayer approach and surface concentration determination. The spatial state of the orientation of ApoH on the lipid layer is investigated by analyzing the process of membrane-attached ApoH molecules being extruded out from the phospholipid monolayer by compression. The results show that on neutral lipid layer ApoH has an upright orientation, which is not sensitive to the phase state of the lipid layer. However, on acidic lipid layer, ApoH may have two forms of orientation. One is an upright orientation in the liquid phase region, and the other is flat orientation on the condensed domain region. The variation of the spatial state of ApoH on the lipid layer may relate to a variety of its physiological functions.
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PMID:Human apolipoprotein H may have various orientations when attached to lipid layer. 1212 80

We have reported that an inhibitor of interleukin-3 (NIL-3) is produced from murine bone marrow cells in response to excess stimulation of interleukin-3. In this report, we attempted the purification of the NIL-3 activity from bone marrow culture supernatant in the presence of interleukin-3. The purified NIL-3 activity was a protein with relative molecular weight of 54.5 kDa (SDS-PAGE), which inhibited the growth of IL-3 dependent DA-1 cell growth in a dose dependent manner. The N-terminal amino acid sequence of purified NIL-3 activity was determined to be homologous to beta-2 glycoprotein I (apolipoprotein H: APO-H). The gene expression of APO-H was detected by nested-PCR in STIL-3 C5-CM stimulated total bone marrow cells and STIL-3 C5-CM stimulated bone marrow fraction 2 (Fr. 2) which has been reported as a hematopoietic stem cell rich fraction. These observations indicate the possibility that the APO-H is the NIL-3 which was produced from bone marrow cells in response to excess IL-3 stimuli.
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PMID:Identification of negative regulator of interleukin-3 (NIL-3) in bone marrow. 1220 49

Hybridomas expressing murine gammadelta T-cell receptors were found to produce cytokines in response to cardiolipin (CL) and structurally related anionic phospholipids. This response required serum at concentrations related to the amount of CL in cultures. The purified serum factor, beta2-glycoprotein 1 (beta2-GP1) (apolipoprotein H), supported the CL response alone, whereas several other serum proteins and ovalbumin did not. beta2-GP1 is known to form complexes with anionic phospholipids, particularly CL, which are often recognized by pathological autoantibodies. We speculate that gammadelta T cells also recognize such complexes and that the hybridoma response reported here reflects this specificity.
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PMID:Hybridomas expressing gammadelta T-cell receptors respond to cardiolipin and beta2-glycoprotein 1 (apolipoprotein H). 1295 Jun 85

Cerebral infarction is the most common arterial thromboembolic complication in the anti-phospholipid antibodies (aPL) syndrome. In an effort to clarify the roles of aPL in the pathogenesis of cerebral infarction in patients with SLE, we examined the levels of anti-cardiolipin/2-glycoprotein I antibodies (anti-CL/beta2-GPI) and anti-phosphatidylserine/prothrombin anti-bodies (anti-PS/PT) in addition to lupus anticoagulant (LA) activity in 126 patients with SLE (35 with cerebral infarction and 91 without thrombosis). Both anti-CL/beta2-GPI and anti-PS/PT strongly correlated with the presence of LA activity. The prevalence of cerebral infarction was obviously higher in the patients who had both anti-CL/beta2-GPI and anti-PS/PT (76.5% [26/34 cases], p<0.0001) than in the other patients having anti-CL/beta2-GPI or anti-PS/PT alone or neither of them (9.8% [9/92 cases]). Furthermore, we studied the in vitro effects of anti-CL/beta2-GPI and/or anti-PS/PT on the enhancement of platelet activation induced by stimulation with a low concentration of adenosine diphosphate (ADP). The purified IgG containing both anti-CL/beta2-GPI and anti-PS/PT caused significant enhancement of platelet activation caused by ADP. However, the purified IgG containing either anti-CL/beta2-GPI or anti-PS/PT had no enhancing effects on it. Furthermore, platelet activation was generated by the mixture of anti-CL/beta2-GPI-IgG and anti-PS/PT-IgG prepared from individual patients, but not by each fraction alone. These results indicate that anti-CL/beta2-GPI and anti-PS/PT may cooperate to promote platelet activation, which may contribute to the risk of cerebral infarction in patients with SLE.
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PMID:Strong correlation between the prevalence of cerebral infarction and the presence of anti-cardiolipin/beta2-glycoprotein I and anti-phosphatidylserine/prothrombin antibodies--Co-existence of these antibodies enhances ADP-induced platelet activation in vitro. 1511 58

Diabetes mellitus (DM) is associated with oxidative stress, elevation of inflammatory markers and other mechanisms, which may contribute to accelerated atherosclerosis. The aim of the study was to determine prominent factors of these pathogenic processes in patients with DM, to examine their relationship in serum, and to find out the differences between DM1 and DM2. Advanced oxidation protein products (AOPP), C-reactive protein (CRP), pregnancy-associated plasma protein-A (PAPP-A), anticardiolipin antibodies (ACA) and anti-beta2-glycoprotein-1 antibodies (anti-beta2-GPI) were determined in 27 patients with DM1, 27 patients with DM2 and 23 healthy subjects. AOPP, CRP and anti-beta2-GPI were significantly elevated in DM2 in comparison with healthy subjects (p<0.01, p<0.0001, p<0.0001, respectively). In DM1, anti-beta2-GPI were elevated (p<0.0001) as well, but there was no increase of either AOPP or CRP. There was no difference in PAPP-A levels in DM1 or DM2 and healthy subjects. In DM 1, AOPP correlate significantly with anti-beta2-GPI (r = 0.68, p<0.05). In DM2, there is a significant correlation between anti-beta2-GPI and PAPP-A (r=0.45, p<0.05). Oxidative stress and inflammation are more expressed in DM2 and they are partly related. In DM1, oxidative stress seems to be in closer link to autoimmune reaction than to inflammation.
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PMID:Oxidative stress, inflammation and autoimmune reaction in type 1 and type 2 diabetes mellitus. 1535 43

Antiphospholipid antibodies detected by lupus anticoagulant, anticardiolipin or anti-beta2 glycoprotein I assays were associated with fetal loss. Rather than being diagnostic tools only, antiphospholipid antibodies are thought to be pathogenic. The strongest demonstration of their pathogenic role lies in the ability to induce fetal resorptions--the experimental equivalents of the human fetal losses--when passively infused in pregnant naive animals. However, still debated is how the antibodies might induce the obstetrical manifestations. Thrombotic events at the placental levels might be related to endothelial cell activation, inhibition of protein C/S system and fibrinolysis as well as to Annexin V displacement. However, the thrombophilic state apparently cannot explain all the miscarriages and a direct antibody-mediated damage on the trophoblast has been suggested. During differentiation to syncytium, trophoblasts express cell membrane anionic phospholipids that can bind beta2 glycoprotein I, the main cationic phospholipid binding protein recognized by the antiphospholipid antibodies. Adhered beta2-glycoprotein I might be recognized by the antibodies that, once bound, strongly interfere with in vitro trophoblast cell maturation so resulting in a defective placentation. These mechanisms have been suggested to play a role in early fetal loss, while thrombotic events would be responsible for miscarriages late in the pregnancy.
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PMID:Antiphospholipid antibodies as cause of pregnancy loss. 1548 95

Complement receptor 2-deficient (Cr2(-/-)) mice are resistant to mesenteric ischemia/reperfusion (I/R) injury because they lack a component of the natural Ab repertoire. Neither the nature of the Abs that are involved in I/R injury nor the composition of the target Ag, to which recognition is lacking in Cr2(-/-) mice, is known. Because anti-phospholipid Abs have been shown to mediate fetal growth retardation and loss when injected into pregnant mice, we performed experiments to determine whether anti-phospholipid Abs can also reconstitute I/R injury and, therefore, represent members of the injury-inducing repertoire that is missing in Cr2(-/-) mice. We demonstrate that both murine and human monoclonal and polyclonal Abs against negatively charged phospholipids can reconstitute mesenteric I/R-induced intestinal and lung tissue damage in Cr2(-/-) mice. In addition, Abs against beta2 glycoprotein I restore local and remote tissue damage in the Cr2(-/-) mice. Unlike Cr2(-/-) mice, reconstitution of I/R tissue damage in the injury-resistant Rag-1(-/-) mouse required the infusion of both anti-beta2-glycoprotein I and anti-phospholipid Ab. We conclude that anti-phospholipid Abs can bind to tissues subjected to I/R insult and mediate tissue damage.
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PMID:Anti-phospholipid antibodies restore mesenteric ischemia/reperfusion-induced injury in complement receptor 2/complement receptor 1-deficient mice. 1555 3


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