Academic literature on the topic 'Phospholipid antibody'
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Journal articles on the topic "Phospholipid antibody":
1
Wu, X. X., and J. H. Rand. "Antiphospholipid antibody-mediated interference with annexin-V anticoagulant activity." Hämostaseologie 21, no. 02 (2001): 50–53. http://dx.doi.org/10.1055/s-0037-1619508.
Abstract:
SummaryThe antiphospholipid (aPL) syndrome is a disorder in which vascular thrombosis and/or recurrent pregnancy losses occur together with serologic and coagulation evidence for antibodies directed against anionic phospholipid-protein complexes. Evidence has been developed for the idea that thrombosis in this syndrome may result from disruption of the binding of annexin-V to the phospholipids which line the placental and systemic vasculatures. We hypothesize that annexin-V, a protein known to have high affinity for anionic phospholipids, plays a thromboregulatory role at the vascular-blood interface by shielding anionic phospholipids from complexation with coagulation proteins in circulating blood. We propose that the thrombotic manifestations of the antiphospholipid syndrome are due to disruption of this annexin-V shield by antiphospholipid antibodies, thereby resulting in a net increase of thrombogenic phospholipids exposed to circulating blood. The accumulated data from tissue immunohistochemistry, trophoblast and endothelial cell culture studies, coagulation studies using noncellular phospholipids, and competition studies on artificial phospholipid bilayer are consistent with the hypothesis that the interference with the binding of annexin-V to anionic phospholipid surfaces plays an important role in the mechanism of thrombosis and in pregnancy loss in the antiphospholipid syndrome.
2
Rauch, J., and AS Janoff. "Antibodies against Phospholipids other than Cardiolipin: Potential Roles for Both Phospholipid and Protein." Lupus 5, no. 5 (October 1996): 498–502. http://dx.doi.org/10.1177/096120339600500534.
Abstract:
Autoantibodies to phospholipids other than cardiolipin have received less attention, to date, than anti-cardiolipin antibodies. This review focuses on these antibodies and potential roles for both phospholipid and protein in their reactivity. We review data in the literature indicating that antibodies to phosphatidylethanolamine and some lupus anticoagulant antibodies recognize phospholipid-binding proteins in association with phospholipid. Kininogens appear to be involved in the binding of antibodies to phosphatidylethanolamine, while phosphatidylserine-binding proteins, such as prothrombin and annexin V, have been implicated in lupus anticoagulant antibody recognition. These proteins bind to phospholipids that normally reside in the inner monolayer of the cell membrane, suggesting that exposure of these lipids is necessary for protein binding and antibody recognition to occur. In contrast, other autoantibodies, in particular those reactive with erythrocytes, appear to be directed at phospholipids that normally occur in the outer membrane leaflet, such as phosphatidylcholine. In summary, there is clearly accumulating evidence that antibodies to phospholipids other than cardiolipin recognize epitopes on phospholipid-binding proteins. It is not clear whether recognition of these epitopes is due to an increase in antigen density or a change in the protein or phospholipid structure, but it is likely that both protein and phospholipid structure play an important role in the in vivo interactions of these antibodies.
3
KOIKE, TAKAO. "Anti-phospholipid antibody syndrome." Nihon Naika Gakkai Zasshi 84, no. 9 (1995): 1569–73. http://dx.doi.org/10.2169/naika.84.1569.
4
Panarelli, P., M. P. Viola-Magni, and E. Albi. "Antiphosphatidylinositol Antibody in Deep Venous Thrombosis Patients." International Journal of Immunopathology and Pharmacology 16, no. 1 (January 2003): 61–66. http://dx.doi.org/10.1177/039463200301600109.
Abstract:
Antiphospholipid antibodies are a heterogeneous group of immunoglobulins with specificity for a number of phospholipids, phospholipid-binding proteins and phospholipid-protein complexes. The association between antiphospholipid antibodies and a variety of pathologic disorders, such as arterial and venous thrombosis and recurrent pregnancy loss is recognized as Antiphospholipid Syndrome. The immunoassay currently used to detect antiphospholipid antibodies is the anticardiolipin test. Anticardiolipin antibodies are believed to be polyspecific antibodies that cross-react with all the anionic phospholipids. Therefore, testing only for anticardiolipin antibodies does not always permit detection of all antiphospholipid antibodies, specially when only IgG are evaluated. In a selected population of 74 idiopathic and secondary deep venous thrombosis patients, IgG anticardiolipin, antiphosphatidylinositol and antiphosphatidylserine antibodies were detected by solid-phase immunoassays. Our results show that by testing for each antiphospholipid family, many patients, not evidenced by the standard anticardiolipin assay, were found to be antiphospholipid-positive. The anticardiolipin positive patients have always low, moderate or high levels of antiphospholipid antibodies, suggesting that the antiphospholipid positivity is predictive of anticardiolipin positivity. It should be noted that the patients with only antiphosphatidylinositol positive antibody have a story of nervous system pathology. The meaning of these results is at present under discussion.
5
Stewart, M. W., W. S. Etches, A. S. Russell, J. S. Percy, C. A. Johnston, C. K. Chew, and P. A. Gordon. "Detection of Antiphospholipid Antibodies by Flow Cytometry: Rapid Detection of Antibody Isotype and Phospholipid Specificity." Thrombosis and Haemostasis 70, no. 04 (1993): 603–7. http://dx.doi.org/10.1055/s-0038-1649636.
Abstract:
SummaryLaboratory diagnosis of antiphospholipid antibodies is important in patients with clinical features of the antiphospholipid syndrome, such as thrombosis and fetal loss. We have developed a novel method for the detection of antiphospholipid antibodies using flow cytometry. Anionic phospholipids cardiolipin, phosphatidylserine and phosphatidylinositol are coated onto polystyrene beads of different sizes, allowing detection and semiquantitation of their respective phospholipid antibody isotypes. The results of the flow cytometric method closely correlate those of the standardised anticardiolipin enzyme-linked immunosorbent assay (ELISA), but the method is quicker and is versatile in its ability to detect IgG, IgM and IgA antibody isotypes at the same time. The method promises to be useful in evaluating the significance of phospholipid specificity and antibody isotypes in patients with the antiphospholipid syndrome.
6
Gupta, Anuj, Joshika Agarwal, Shilpi Gupta, and Anurag Singh. "Clinical significance of anti-phospholipid antibodies in Henoch Schönlein purpura." International Journal Of Community Medicine And Public Health 8, no. 8 (July 27, 2021): 4037. http://dx.doi.org/10.18203/2394-6040.ijcmph20213041.
Abstract:
Background: Henoch Schönlein purpura also known as IgA vasculitis is described histologically by IgA deposition in the blood vessel walls and presents with kidney involvement, palpable purpura, arthralgia, and abdominal pain. Our study aims to evaluate the association between anti-phospholipid antibody, anti-cardiolipin antibody, anti-beta(2) glycoprotein 1 antibody and Anti-phosphatidylserine/prothrombin antibodies and IgA vasculitis. Treatment response with intravenous steroids and cyclophosphamide was also studied based on resolution of antibody titer.Methods: We conducted an observational study in three Rheumatology clinics at Ahmedabad, India. Data was collected for a period of 6 months. Diagnosis of IgA vasculitis was determined based on the International Chapel hill consensus conference 2012. Disease activity was assessed based on antibody titer, histological grading and through a pre-determined clinical form to assess objective clinical symptoms. P value of less than 0.05 was considered significantResults: Study evaluated antibody titer of 178 patients. Sixty one percent of the patient's had positive anti-phospholipid antibody titer with predominant antibody subtype as IgG. Inflammatory markers were significantly higher in patient having anti-phospholipid antibody titer. Anti-phospholipid antibody was present in 100 percent patients who had vascular thrombosis. IgG subtype of anti-cardiolipin antibody were found in 60 percent of the patients with renal complication.Conclusions: Anti-phospholipid antibody have a close association with IgA vasculitis. Anti-phospholipid antibody has a significant role in mounting inflammatory response and vascular thrombosis. Combination treatment of intravenous steroids and cyclophosphamide found to be more effective in resolution of titer
7
Wittevrongel, C., M. Vanrusselt, M. Hoylaerts, J. Vermylen, and J. Arnout. "Beta-2-glycoprotein I Dependent Lupus Anticoagulants Form Stable Bivalent Antibody Beta-2-Glycoprotein I Complexes on Phospholipid Surfaces." Thrombosis and Haemostasis 79, no. 01 (1998): 79–86. http://dx.doi.org/10.1055/s-0037-1614224.
Abstract:
SummaryThe precise mechanism by which Beta-2-glycoprotein I (β2GPI-) dependent lupus anticoagulants lengthen phospholipid-dependent clotting reactions is still poorly understood. In order to study this, murine monoclonal antibodies (moabs) against human β2GPI were raised. Eight of the 21 anti-β2GPI moabs, obtained from 2 fusions, fulfilled the criteria for lupus anticoagulant (LA) activity as tested with a variety of sensitive screening assays and confirmatory tests. Seven moabs did not influence any clotting test. The LA positive moabs were found to compete for similar or closely spaced epitopes on immobilized β2GPI. Two moabs with potent LA activity (moabs 22 F 6 and 22 B 3) and 1 moab without LA activity (moab 16 B 3) were selected to study the interaction between antibody, β2GPI and phospholipid. Interactions were investigated by real-time biospecific interaction analysis (BIA) based on plasmon surface resonance technology on a BIA-core instrument using a sensor chip coated with phospholipid. When 22 F 6, the moab with the most pronounced LA activity, was allowed to interact with the phospholipid surface at concentrations between 0 and 400 nmol/l, no appreciable binding could be detected. Likewise, no binding could be measured when β2GPI at concentrations between 0 and 400 nmol/l was passed over the phospholipid coated sensor chip. Combinations of β2GPI and 22 F 6 resulted in significant binding. Similar results were obtained with 22 B 3, another moab with LA activity. A LA negative Moab, 16 B 3, did not cause binding of antibody-β2GPI complexes. Fab’ fragments, derived from moab 22 F 6, inhibited the binding of β2GPI-22 F 6 and β2GPI-22 B 3 in a concentration dependent way, indicating that only bivalent β2GPI-antibody complexes bind with high affinity to phospholipids. Fab’ fragments, derived from moab 22 F 6, also inhibited the LA effect of moabs 22 F 6 and 22 B 3 in diluted plasma. In summary, these experiments indicate that the β2GPI-dependent LA effect depends on the formation of bivalent β2GPI-antibody complexes on phospholipid surfaces.
8
MATSUURA, EIJI. "Homologous antigen of anti-phospholipid antibody." Japanese Journal of Clinical Immunology 16, no. 6 (1993): 537–44. http://dx.doi.org/10.2177/jsci.16.537.
9
Kittisupamongkol, W. "The hidden anti-phospholipid antibody syndrome." QJM 101, no. 7 (March 4, 2008): 591. http://dx.doi.org/10.1093/qjmed/hcn063.
10
Taylor, Pamela V., Sylvia M. Skerrow, and Christopher W. G. Redman. "Pre-eclampsia and anti-phospholipid antibody." BJOG: An International Journal of Obstetrics and Gynaecology 98, no. 6 (June 1991): 604–6. http://dx.doi.org/10.1111/j.1471-0528.1991.tb10382.x.
Dissertations / Theses on the topic "Phospholipid antibody":
1
Gatenby, Paul, Gytis Danta, Roger Tuck, Colin Andrews, and Carolyn Hawkins. "Cerebrovascular disease associated with antiphospholipid antibodies: more questions than answers." Master's thesis, BioMed Central, 2006. http://hdl.handle.net/10440/104.
Abstract:
Neurological syndromes occur in a significant number of patients with antiphospholipid antibodies. The
optimal management for these patients however remains uncertain.
Our study is a descriptive analysis looking retrospectively at 45 patients who presented to the principal
tertiary referral centre in the Australian Capital Territory, with either cerebral arterial or venous
thrombosis for which there was no obvious cause for their presentation when initially reviewed. The
diagnosis was based on the clinical findings made by one of three neurologists attached to our centre.
Radiological findings and the presence of either IgM or IgG anticardiolipin antibodies, IgG anti-beta-2
glycoprotein 1 antibodies or a lupus anticoagulant were then documented.
In this group of patients three subgroups were identified:
1. Individuals that fulfilled the Sapporo Classification Criteria
2. Individuals with transiently positive antiphospholipid antibodies and
3. Individuals with persistently low positive antiphospholipid antibodies.
The most interesting of these three groups are those individuals with transiently positive antiphospholipid
antibodies. A potential cause for presentation was identified in only one patient of this group with
documented infective endocarditis and bacteraemia. Comparison with the other two groups suggested
that there was little in terms of clinical presentation, radiological findings or intercurrent risk factors for
thrombotic disease to distinguish between them. With disappearance of antiphospholipid antibodies, the
individuals within this group have not had further thrombotic events.
Our observations emphasise the problems that continue to exist in relation to the occurrence of
cerebrovascular disease in the context of antiphospholipid antibodies and the optimal management of
these stratified groups. Our findings also raise an as yet unanswered question as to the signficance of these
transiently positive antiphospholipid antibodies. In the absence of significant intercurrent risk factors our
findings would suggest that in the group we describe that they are likely to be of clinical significance.
2
Paavola, T. (Timo). "Associations of low HDL cholesterol level and premature coronary heart disease with functionality and phospholipid composition of HDL and with plasma oxLDL antibody levels." Doctoral thesis, Oulun yliopisto, 2019. http://urn.fi/urn:isbn:9789526223360.
Abstract:
Abstract Coronary heart disease (CHD) is a clinical manifestation of atherosclerosis. It is a major cause of mortality and morbidity both in Finland and globally. Even after the best known treatments a significant residual risk of CHD remains. A low plasma HDL cholesterol level (HDL, high-density lipoprotein) is a common lipid abnormality in patients affected by premature CHD and also a component of the metabolic syndrome, a cluster of risk factors for atherosclerosis associated with central obesity. In this study, a phenotype of low HDL cholesterol level and premature CHD was investigated in two Northern Finnish family populations. The aim was to find new biological factors accounting for the elevated CHD risk in the phenotype. In the subjects of family population I, plasma levels of antibodies (IgG, IgM, IgA) against experimental epitopes (malondialdehyde-acetaldehyde-modified, copper-oxidized) of oxidized LDL (low-density lipoprotein) particles were measured. In the subjects of family population II, capacity of HDL fractions (total HDL, HDL2 and HDL3) to accept cholesterol from a THP-1 experimental foam cell model was assayed (cholesterol efflux). In addition, a phospholipid composition of their HDL fractions (HDL2 and HDL3) was measured using liquid chromatography-mass spectrometry. The antibody levels were not related to CHD or to HDL cholesterol level. Instead, the cholesterol efflux to HDL2 fraction was clearly impaired in CHD, which was associated with the low HDL cholesterol level of the patients. The impaired cholesterol efflux to HDL2 fraction was primarily in conjunction with the metabolic syndrome. The phospholipid composition of HDL fractions was different between the affected and the non-affected subjects. As an example, characteristic of the metabolic syndrome were elevated contents of palmitic, palmitoleic or oleic acids relative to linoleic acid in lysophosphatidylcholines and phosphatidylcholines. In conclusion, the HDL fraction is both functionally and compositionally modified in the phenotype of low HDL cholesterol level and premature CHD. Especially the cholesterol efflux capacity of the HDL2 fraction and thus its many functional properties may be impaired. There are many characteristic features in the phospholipid composition of the HDL in the phenotype which were detected in HDL2 and HDL3 fractionsTiivistelmä Sepelvaltimotauti on ateroskleroosin kliininen ilmenemismuoto. Se on merkittävimpiä kuolleisuuden ja sairastavuuden aiheuttajia niin Suomessa kuin maailmalla. Parhaillakin tunnetuilla hoidoilla sepelvaltimotaudille jää huomattava jäännösriski. Plasman matala HDL-kolesterolitaso (HDL, high-density lipoprotein) on yleinen lipidipoikkeavuus varhaista sepelvaltimotautia sairastavilla ja myös eräs metabolisen oireyhtymän, eli keskivartalolihavuuteen liittyvän ateroskleroosin riskitekijäkasauman, komponentti. Tässä väitöskirjassa tutkittiin matalan HDL-kolesterolitason ja varhaisen sepelvaltimotaudin fenotyyppiä kahdessa pohjoissuomalaisessa sukuaineistossa. Tavoitteena oli löytää uusia biologisia tekijöitä fenotyypin kohonneen sepelvatimotautiriskin taustalta. Ensimmäisen aineiston henkilöiden plasmasta mitattiin vasta-ainetasoja (IgG, IgM, IgA) LDL-hiukkasten (LDL, low-density lipoprotein) kokeellisia hapettuneita epitooppeja (malonidialdehydi-asetaldehydi-modioitu ja kuparilla hapetettu LDL) vastaan. Toisessa aineistossa mitattiin henkilöiden HDL-fraktioiden (kokonais-HDL, HDL2 ja HDL3) kykyä saada aikaan kolesterolin ulosvirtausta kokeellisesta THP-1 vaahtosolumallista. Lisäksi heidän HDL-fraktioidensa (HDL2, HDL3) fosfolipidikoostumus mitattiin nestekromatografi-massaspektrometri-laitteistolla. Vasta-ainetasot eivät liittyneet sepelvaltimotautiin tai HDL-kolesterolitasoon. Sen sijaan kolesterolin ulosvirtaus HDL2-fraktioon oli selkeästi alentunut sepelvaltimotaudissa, mikä liittyi potilaiden pieneen HDL-kolesterolipitoisuuteen. Alentunut ulosvirtaus HDL2-fraktioon liittyikin ensisijaisesti metaboliseen oireyhtymään. HDL-fraktioiden fosfolipidikoostumus erosi terveiden ja sairaiden välillä. Esimerkiksi metabolisessa oireryhtymässä tunnusomaista oli lysofosfatidyylikoliinien ja fosfatidyylikoliinien sisältämän palmitiinihapon, palmitoleiinihapon tai oleiinihapon suurentunut määrä suhteessa niiden sisältämän linoleenihapon määrään. Loppupäätelmä on, että matalan HDL-kolesterolitason ja varhaisen sepelvaltimotaudin fenotyypin HDL-fraktio on sekä toiminnaltaan että koostumukseltaan muuntunut. Erityisesti HDL2-fraktion kyky saada aikaan kolesterolin ulosvirtausta ja näin ollen sen monet toiminnalliset ominaisuudet voivat olla alentuneet. Fenotyypin HDL:n fosfolipidikoostumuksessa on monia tunnusomaisia piirteitä, joita havaittiin sekä HDL2- että HDL3-fraktiossa
3
Letourneur, Didier. "Polymères fonctionnels phosphorylés : interactions biospécifiques avec des protéines humaines, anticorps anti-adn, antiphospholipides et facteurs de transcription." Paris 13, 1988. http://www.theses.fr/1988PA132010.
Abstract:
Des résines dérivées du polystyrene réticule ont été synthétisées. Ces polymères sont fonctionnalisés par des groupements chimiques analogues à ceux de l'adn et des phospholipides. L'affinité biospécifique de ces resines pour des protèines humaines qui admettent pour substrat l'adn et les phospholipides : anticorps anti adn, anti phospholipide, facteurs de transcription de l'adn. Les anticorps qui sont présents dans le sang des patients atteints de lupus érythemateux dissemine (l. E. D) ont montré une affinité spécifique tres élevée pour les dérivés fonctionnels du polystyrene;ces interactions impliquent le fragment fab des immunoglobulines lupiques et des sites distribués de façon statistique à la surface des polymères. Les polymères fonctionnels phosphoryles permettent en tant que phase stationnaire la résolution chromatographique d'extraits cellulaires contenant des facteurs de transcription de l'adn
Books on the topic "Phospholipid antibody":
1
Khamashta, Munther A., Graham R. V. Hughes, and Guillermo Ruiz-Irastorza. Anti-phospholipid antibody syndrome. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0120.
Abstract:
The anti-phospholipid syndrome (APS) described almost 30 years ago, is now recognized as a major cause of deep vein thrombosis, stroke, and heart attacks in young people (<45 years of age). It is also the commonest treatable cause of recurrent miscarriages and a major cause of late fetal death. Other clinical manifestations are cardiac valvular disease, livedo reticularis, renal thrombotic microangiopathy, thrombocytopenia, haemolytic anaemia, epilepsy, and cognitive impairment. The presence of anti-phospholipid antibodies (aPL) has been closely related to the development of thrombosis and complications in pregnancy. However, not all patients with aPL will develop the clinical features. Lupus anticoagulant is generally thought to be more strongly associated with the risk of clinical manifestations of APS than anticardiolipin and anti ?2-glycoprotein I antibodies. The exact pathogenic mechanisms leading to thrombosis and/or pregnancy morbidity are poorly understood. Therapy of thrombosis is based on long-term oral anti-coagulation and patients with arterial events should be treated aggressively. Obstetric care is based on combined medical-obstetric high-risk management and treatment with aspirin and heparin.
2
Khamashta, Munther A., Graham R. V. Hughes, and Guillermo Ruiz-Irastorza. Anti-phospholipid antibody syndrome. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0120_update_001.
Abstract:
The anti-phospholipid syndrome (APS) described almost 30 years ago, is now recognized as a major cause of deep vein thrombosis, stroke, and heart attacks in young people (<45 years of age). It is also the commonest treatable cause of recurrent miscarriages and a major cause of late fetal death. Other clinical manifestations are cardiac valvular disease, livedo reticularis, renal thrombotic microangiopathy, thrombocytopenia, haemolytic anaemia, epilepsy, and cognitive impairment. The presence of anti-phospholipid antibodies (aPL) has been closely related to the development of thrombosis and complications in pregnancy. However, not all patients with aPL will develop the clinical features. Lupus anticoagulant is generally thought to be more strongly associated with the risk of clinical manifestations of APS than anticardiolipin and anti ?2-glycoprotein I antibodies. The exact pathogenic mechanisms leading to thrombosis and/or pregnancy morbidity are poorly understood. Therapy of thrombosis is based on long-term oral anti-coagulation and patients with arterial events should be treated aggressively. Obstetric care is based on combined medical-obstetric high-risk management and treatment with aspirin and heparin.
3
Hamann, Philip, and Neil McHugh. Autoimmune serology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0063.
Abstract:
Autoimmune serology has become central in the characterization of many rheumatic conditions and in many cases the presence of an autoantibody (e.g. anti-citrullinated peptide, rheumatoid factor, ANCA, ANA, ENA, anti-phospholipid antibody), may form part of the diagnostic criteria. Increasingly, as pathogenic mechanisms are derived, the role of these autoantibodies is becoming better understood. This chapter covers the key techniques (immunoflourescence, immunodiffusion, ELISA, immunoblotting, immunoprecipitation) used in autoantibody detection as well as the clinico-pathological significance of a positive result.
4
Hamann, Philip, and Neil McHugh. Autoimmune serology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0063_update_002.
Abstract:
Autoimmune serology has become central in the characterization of many rheumatic conditions and in many cases the presence of an autoantibody (e.g. anti-citrullinated peptide, rheumatoid factor, ANCA, ANA, ENA, anti-phospholipid antibody), may form part of the diagnostic criteria. Increasingly, as pathogenic mechanisms are derived, the role of these autoantibodies is becoming better understood. This chapter covers the key techniques (immunoflourescence, immunodiffusion, ELISA, immunoblotting, immunoprecipitation) used in autoantibody detection as well as the clinico-pathological significance of a positive result.
5
Thornton, Clare, and Justin Mason. Vascular biology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0057.
Abstract:
Vascular biology is the study of the physiology of the vasculature and how it may be the target for disease processes. An understanding of vascular biology is central to the study of rheumatic disease for three reasons: it is an integral part of a functioning immune system; it is the primary site of pathology in many conditions; and it is the site of the important secondary complications of chronic inflammation, endothelial dysfunction and atherosclerosis. Vascular biology requires a detailed knowledge of the anatomy and physiology of the vasculature and its constituent vessels. The multistep process by which leucocytes interact with endothelium lining postcapillary venules in order to leave the circulation and migrate towards a site of inflammation is central to the pathology of inflammatory disease. The vasculature is the primary site of injury in several rheumatic diseases, including the vasculitides. It may also be damaged by chronic inflammation, leading to endothelial dysfunction and accelerated atherosclerosis. Thrombosis is also a critical pathological process in several chronic inflammatory diseases, particularly the anti-phospholipid antibody syndrome and Behçet's syndrome. The vascular endothelium is central to angiogenesis, the process of new capillary outgrowth, upon which synovial proliferation in inflammatory arthritis is dependent. Angiogenesis is inhibited by current anti-rheumatic therapies and may become a target for novel anti-rheumatic drugs. An increasing area of research concerns the direct effects of drugs used in the treatment of atherosclerosis and inflammatory disease on the endothelium, and whether these agents are beneficial or harmful. Of particular interest to rheumatologists are the vascular effects of statins, disease-modifying anti-rheumatic drugs (DMARDs), immunosuppressants, and cyclooxygenase inhibitors.
6
Thornton, Clare, and Justin Mason. Vascular biology. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0057_update_001.
Abstract:
Vascular biology is the study of the physiology of the vasculature and how it may be the target for disease processes. An understanding of vascular biology is central to the study of rheumatic disease for three reasons: it is an integral part of a functioning immune system; it is the primary site of pathology in many conditions; and it is the site of the important secondary complications of chronic inflammation, endothelial dysfunction and atherosclerosis. Vascular biology requires a detailed knowledge of the anatomy and physiology of the vasculature and its constituent vessels. The multistep process by which leucocytes interact with endothelium lining postcapillary venules in order to leave the circulation and migrate towards a site of inflammation is central to the pathology of inflammatory disease. The vasculature is the primary site of injury in several rheumatic diseases, including the vasculitides. It may also be damaged by chronic inflammation, leading to endothelial dysfunction and accelerated atherosclerosis. Thrombosis is also a critical pathological process in several chronic inflammatory diseases, particularly the anti-phospholipid antibody syndrome and Behçet’s syndrome. The vascular endothelium is central to angiogenesis, the process of new capillary outgrowth, upon which synovial proliferation in inflammatory arthritis is dependent. Angiogenesis is inhibited by current anti-rheumatic therapies and may become a target for novel anti-rheumatic drugs. An increasing area of research concerns the direct effects of drugs used in the treatment of atherosclerosis and inflammatory disease on the endothelium, and whether these agents are beneficial or harmful. Of particular interest to rheumatologists are the vascular effects of statins, disease-modifying anti-rheumatic drugs (DMARDs), immunosuppressants, and cyclooxygenase inhibitors.
Book chapters on the topic "Phospholipid antibody":
1
Meroni, Pier Luigi, and Cecilia B. Chighizola. "Anti-phospholipid Antibody Mechanisms of Thrombosis." In Encyclopedia of Medical Immunology, 63–70. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-0-387-84828-0_420.
2
Al-Osaimi, Hanan, and Areej Althubiti. "Gestational Rheumatology." In Skills in Rheumatology, 383–406. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-8323-0_17.
Abstract:
AbstractThere are changes that occur in the maternal organ systems due to increased demands of pregnancy. Most of the rheumatic disorders occur in the reproductive age group. The hormonal changes that occur during pregnancy may mimic the signs and symptoms of rheumatic disorders thereby making the diagnosis difficult. Rheumatological disorders need to be diagnosed and treated at least 6 months before the onset of pregnancy; otherwise they may have considerable effect on the prognosis of the disease. This is particularly evident in cases of SLE and anti-phospholipid antibody syndrome. Therefore, pregnancy is a crucial issue that needs to be clearly addressed in details in all female patients in the reproductive age group having some of the rheumatological disorders.
3
Roubey, R. A. S. "Antiphospholipid Antibody-negative Syndrome — Other Phospholipids." In Hughes Syndrome, 253–60. London: Springer London, 2000. http://dx.doi.org/10.1007/978-1-4471-3666-8_26.
4
Umeda, Masato, Koji Igarashi, Shigeru Tokita, Farooq Reza, and Keizo Inoue. "Anti-Phosphatidylserine Monoclonal Antibody: Structural Template for Studying Lipid-Protein Interactions and for Identificationo of Phosphatidylserine Binding Proteins." In Phospholipids and Signal Transmission, 219–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-662-02922-0_18.
5
Khamashta, Munther A., Graham R. V. Hughes, and Guillermo Ruiz-Irastorza. "Anti-phospholipid antibody syndrome." In Oxford Textbook of Rheumatology, 957–68. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0120_update_002.
Abstract:
The anti-phospholipid syndrome (APS) described almost 30 years ago, is now recognized as a major cause of deep vein thrombosis, stroke, and heart attacks in young people (<45 years of age). It is also the commonest treatable cause of recurrent miscarriages and a major cause of late fetal death. Other clinical manifestations are cardiac valvular disease, livedo reticularis, renal thrombotic microangiopathy, thrombocytopenia, haemolytic anaemia, epilepsy, and cognitive impairment. The presence of anti-phospholipid antibodies (aPL) has been closely related to the development of thrombosis and complications in pregnancy. However, not all patients with aPL will develop the clinical features. Lupus anticoagulant is generally thought to be more strongly associated with the risk of clinical manifestations of APS than anticardiolipin and anti ?2-glycoprotein I antibodies. The exact pathogenic mechanisms leading to thrombosis and/or pregnancy morbidity are poorly understood. Therapy of thrombosis is based on long-term oral anti-coagulation and patients with arterial events should be treated aggressively. Obstetric care is based on combined medical-obstetric high-risk management and treatment with aspirin and heparin.
6
Pattison, N. S., and W. F. Lubbe. "Treatment of Anti-Phospholipid Antibody Mediated Fetal Loss: The Case for Corticosteroid Therapy." In Phospholipid-Binding Antibodies, 323–34. CRC Press, 2020. http://dx.doi.org/10.1201/9780429278129-24.
7
Hamann, Philip, and Neil McHugh. "Autoimmune serology." In Oxford Textbook of Rheumatology, 456–62. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0063_update_003.
Abstract:
Autoimmune serology has become central in the characterization of many rheumatic conditions and in many cases the presence of an autoantibody (e.g. anti-citrullinated peptide, rheumatoid factor, ANCA, ANA, ENA, anti-phospholipid antibody), may form part of the diagnostic criteria. Increasingly, as pathogenic mechanisms are derived, the role of these autoantibodies is becoming better understood. This chapter covers the key techniques (immunoflourescence, immunodiffusion, ELISA, immunoblotting, immunoprecipitation) used in autoantibody detection as well as the clinico-pathological significance of a positive result.
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Shil, Rajish Sanjit Kumar, Amal Abdallah Al Dhuhoori, Vipin Mughilassery Thomachan, Jamal Ali Teir, and Renganathan Radhakrishnan. "Anti-Phospholipid Antibody Syndrome Presenting with Seizure and Atrial Mass: A Case Report." In Highlights on Medicine and Medical Science Vol. 2, 84–91. Book Publisher International (a part of SCIENCEDOMAIN International), 2021. http://dx.doi.org/10.9734/bpi/hmms/v2/8354d.
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Thornton, Clare, and Justin Mason. "Vascular biology." In Oxford Textbook of Rheumatology, 415–23. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0057_update_002.
Abstract:
Vascular biology is the study of the physiology of the vasculature and how it may be the target for disease processes. An understanding of vascular biology is central to the study of rheumatic disease for three reasons: it is an integral part of a functioning immune system; it is the primary site of pathology in many conditions; and it is the site of the important secondary complications of chronic inflammation, endothelial dysfunction and atherosclerosis. Vascular biology requires a detailed knowledge of the anatomy and physiology of the vasculature and its constituent vessels. The multistep process by which leucocytes interact with endothelium lining postcapillary venules in order to leave the circulation and migrate towards a site of inflammation is central to the pathology of inflammatory disease. The vasculature is the primary site of injury in several rheumatic diseases, including the vasculitides. It may be damaged by chronic inflammation, leading to endothelial dysfunction and accelerated atherosclerosis. Thrombosis represents a critical pathological process in several chronic inflammatory diseases, particularly the anti-phospholipid antibody syndrome and Behçet’s syndrome. The vascular endothelium is central to angiogenesis, the process of new capillary outgrowth, upon which synovial proliferation in inflammatory arthritis is dependent. Angiogenesis is inhibited by current anti-rheumatic therapies and may become a target for novel anti-rheumatic drugs. An increasing area of research concerns the direct effects of drugs used in the treatment of atherosclerosis and inflammatory disease on the endothelium, and whether these agents are beneficial or harmful. Of particular interest to rheumatologists are the vascular effects of statins, disease-modifying anti-rheumatic drugs (DMARDs), immunosuppressants, and cyclooxygenase inhibitors.
Conference papers on the topic "Phospholipid antibody":
1
Triplett, D. A., J. T. Brant, K. Musgrave, and C. A. Orr. "RELATIONSHIP BETWEEN LUPUS ANTICOAGULANTS AND ANTIBODIES TO PHOSPHOLIPID." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643657.
Abstract:
The relationship of lupus anticoagulants (LA's) to antibodies (IgG and IgM) to cardiolipin (CL), phosphatidylserine (PS), phosphatidylinositol (PI) and phosphatidic acid (PA), detected by an enzyme linked immunoassay, was examined in a series of 100 patients with well characterized LA's. 73% of patients demonstrated antibodies to one or more phospholipids; 62% were positive for CL, 57% were positive for PS, 57% were positive for PI, and 51% were positive for PA. Of the samples with antibodies to phospholipid, 32% had IgG type antibody only, 16% had IgMonly, and 52% had both IgG and IgM antibodies. Of the 100 patients,19% had a history of thrombosis, 8% had ahistory of spontaneous abortion, and 6% had a history of seizure disorder. These complications occurred in the presence (61%) and absence (39%) of detectable phospholipid antibodies. Drug-related LA's were observed in 34 patients; of these 74% were positivefor antiphospholipid antibodies and 24% hada history of thrombosis.The distribution of antibody types with drug-related LA's was similarto the overall group, with 40% IgG only, 8%IgM only and 52% both IgG and IgM These findings indicate that IgG and IgM antibodies to phospholipid are not observed in all patients with lupus anticoagulants, that thrombosis does occur in this population in the absence of detectable antibodies to phospholipid and that drug-related LA's are associated with thrombosis. Furthermore, there appeared to be little relationship between the degree of prolongation of the aPTT and the titer of anti-phospholipid antibody.
2
Kemball-Cook, G., S. J. A. Edwards, K. Sewerin, L.-O. Andersson, and T. W. Barrowcliffe. "THE PHOSPHOLIPID-BINDING SITE OF FACTOR VIII IS LOCATED ON THE 80 kD LIGHT CHAIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643615.
Abstract:
The binding of Factoi. VIII (F.VIII) peptides to phospholipid (PL) vesicles has been studied by two different methods involving the use of fractionated anti-F.VIII:C I-Fab123’pre viously reported, i-Fab123’ was fractionated by immunoadsorptionwith F.VIII-PL complexes into two pools:one binding only to PL-binding sites on F.VIIIsAg (PL-site antibody), the other directed against other antigenic sites (non-PL-site antibody).The first technique used was a modification of the method of Weinstein et al. (Proc.Natl.Acad.Sci.USA, 78, 5137-5141, 1981), and involved incubation of the two anti-F.VIII pool swith F.VIII-containing samples, followed by electrophoretic separation of the complexes on the basis of size in non-denaturing SDS gels: this technique allows qualitative analysis of antibody reactive peptides in highly impure samples. Non-PL-site pool reacted with a range of peptides with MrMapparent Mr 90 kD up to 280 kD, a similar pattern to that of ’heavy chain’(HC) peptides of F.VIII seen on SDS-PAGE under reducing conditions; the PL-site antibody, however, reacted only with peptides at apparent Mrs of 80 kD and sometimes150 kD, but not with bands of higher Mr a pattern more consistent with binding to light chain (LC) peptides. Thesame patterns with the two labels were seen in both plasma and F.VIII concentrateThe second approach employed the two labels described above in direct immunoradiometric assays (IFMA’s) on purified human F.VIII peptides prepared by immunoaffinity chromatography and ion exchange on Mono Q gel. Both PL-site and non-PL-site labels measured similar amounts of F.VIII m a sample containing both HC and LC peptides; however, on assaying a sample containing purified HC peptides alone, PL-site antibody measured only 2% of F.VIII:Ag found by non-PL-site label, indicating that PL-binding sites present in samples containing both HC and LC are absent in HC alone.Results from both these immunological methods indicate that the 80 kD LC peptide of F.VIII carries the PL-binding site.
3
Harris, EN, RA Asherson, E. Baguley, M. Ridley, and GRV Hughes. "A STANDARD ANTI-CARDIOLIPIN (aCL) TEST: USEFULNESS IN IDENTIFICATION OF THE ANTI-PHOSPHOLIPID SYNDROME." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644235.
Abstract:
Some, but not all, patients with the lupus anticoagulant and anti-cardiolipin antibodies are prone to thrombosis, fetal loss and thrombocytopenia. It will be important to identify the particular sub-group of patients with anti-phospholipid (aPL) antibodies most subject to these clinical disorders. A preliminary study has shown that the level of IgG aCL antibody is predicitive for thrombosis, fetal loss, and thrombocytopenia but it will be difficult to substantiate (or refute) these findings unless there is a uniform system to measure aCL antibody levels.Five test sera with defined IgG and IgM aCL levels are currently available to laboratories wishing to standardise the aCL test. The concentrations of aCL in these sera cover the full sensitive range of aCL solid phase assays. Using these. 5 test sera to calibrate our assay system, sera from 3000 patients were analysed: 1400 healthy adults and 1600 consecutive patients with autoimmune disorders. All sera from healthy adults had aCL levels below 10GPL (IgG aCL) or below 10MPL (IgM aCL) units. Of the 1600 autoimmune patients, 115 had levels above 5 GPL and/ or 5MPL units. More than 2/3 of patients with IgG aCL levels above 20 GPL units (30 patients) had thrombosis or fetal loss, but the frequency of these disorders decreased in the 10-20 GPL and 5-10 GPL unit groups. Of the 9 patients with IgM aCL levels above 15 MPL units, 6 had thrombosis or fetal loss.The availability of reference sera to measure IgG and IgM aCL antibody levels may better enable multicenter studies to be performed. A relatively uniform system of measurement may also enable easier identification and management of patients with the anti-phospholipid syndrome.
4
Brien, W., G. Denome, and B. O’Keefe. "THE PREVELANCE OF ANTIPHOSPHOLIPID ANTIBODIES, BY ELISA TECHNIQUE, IN PATIENTS WITH THE LUPUS ANTICOAGULANT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644234.
Abstract:
Patients with the Lupus Anticoagulant and/or anticardiolipin antibodies have been reported to be at increased risk of thrombosis and miscarriages. It has been proposed that the lupus anticoagulant is an antiphospholipid antibody.We evaluated 16 patients with the lupus anticoagulant for the presence of antiphospholipid antibodies. The lupus anticoagulant was documented by the presence of an abnormal APTT, abnormal mixing studies, positive tissue thromboplastin inhibition test and positive platelet neutralization test.Plasma from each patient was assessed for the presence of anticardiolipin, antiphosphatidylserine and antiphosphatidyl-glycerol antibodies by ELISAtechniques. As a control, a neutral phospholipid phosphatidylethanolamine was used. A positive result was established when a delta value of lipid minus control was greater than 3SD compared to a normal population (20 pt.).Using three different patient dilutions, positive results were obtained in 10/16 pt. for anticardiolipin, 11/16 pt. for antiphosphatidylserine and 5/16 pt. for antiphosphatidyl-glycerol antibodies. Three patients were negative for all lipids. If a neutral phospholipid was not used and a delta volume not obtained, 15/16 patients would have had positive results.Our results suggest 1) Not all patients with the Lupus Anticoagulant have antiphosphilipid antibodies by ELISA technique. In evaluating patients with thrombosis and/or miscarriages, both tests should be performed.2) Anticardiolipin antibodies are not present in all patients and with a panel of other negatively charged phospholipids more positive results are obtained. 3) A neutral lipid should be used as a control for non-specific binding of antibody and delta values obtained to see if the results obtained is truly against the negatively charged lipid.
5
Maria, Naomi I., Shani Martinez, Chirag Raparia, Zhengzi Yi, Haiou Tao, Ke Lin, Weijia Zhang, and Anne Davidson. "1001 A new model of spontaneous anti-phospholipid antibody induced pregnancy loss in mice over-expressing human TLR8." In LUPUS 21ST CENTURY 2022 CONFERENCE, Abstracts of Sixth Scientific Meeting of North American and European Lupus Community, Tucson, AZ, USA – September 20–23, 2022. Lupus Foundation of America, 2022. http://dx.doi.org/10.1136/lupus-2022-lupus21century.61.
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Bloom, J. W. "LIPID BINDING PROPERTIES OF HIGHLY PURIFIED rDNA FACTOR VIII." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644041.
Abstract:
The binding of purified rDNA Factor VIII:c to lipid was examined by an ELISA technique. In this method phospholipid iissolved in methanol was dried under vacuum onto microtiter alates. Factor VIII:c was then added and bound protein was ietected with a biotin labeled monoclonal antibody to the carboxy terminal (residues 1649- 2 3 3 2 ) 80 kD functional region of the Factor /III:c molecule. This was followed by strepavidin-peroxidase and substrate addition. Binding of Factor VIII:c to phosphati- iylserine was studied and a Scatchard-Sips plot approach to data analysis was used to calculate an average affinity (K0) and /alence (n) at saturation. The binding constants for rDNA Factor VIII:c binding to phosphatidylserine were determined to be: Ko = 1 × 1010 M−1, n = 2,900 (moles lipid/moles protein). Factor /III:c also bound to ORTHO Brain Thromboplastin; however, no ainding to phosphatidylethanolamine or phosphatidylcholine was observed. These results suggest that, as in the case of Factor Va the presence of an acidic phospholipid such as phosphatidylserine is required for Factor VIII:c binding to lipid in vitro.
7
Lepine, Z., A. Mathian, M. Pineton De Chambrun, F. Cohen, J. Haroche, M. Hie, M. Pha, and Z. Amoura. "SAT0467 Cerebral venous thrombosis occurrence in systemic lupus erythematosus without anti-phospholipid antibody syndrome: a monocentric serie of 10 cases." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.4187.
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Criel, A., B. Gilbert, A. Van Hoof, M. Hidajat, and A. Louwagie. "COMPARISION OF THE DETECTION OF LUPUS ANTICOAGULANTS USING THREE DIFFERENT METHODS AND THE PRESENCE OF ANTI-CARDIOLIPIN ANTIBODIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644233.
Abstract:
Lupus anticoagulant (LAC) is an antibody directed against phospholipids which prolongs in vitro clotting assays. Several detection methods have been described; however all give some different results. Recently ELISA and RIA assays have been developed which detect IgG and IgM anti-cardiolipin antibodies. The aim of our study was to compare three different LAC tests with an ELISA anti-cardiolipin test. The tests used were : kaolin clotting time (KCT or Exnertest), tissue thromboplastin inhibition test (TTI or Schleider test), activated partial thromboplastin time using a 50, 100, 200 fold dilution of the phospholipid preparation (APTT dilution test), and an IgG and IgM anti-cardiolipin ELISA test. 114 samples of patients suffering from diseases known to be accompanied with LAC antibodies (auto-immune diseases, recurrent abortion, thromboembolism, etc.) were studied. Positivity with one of the tests was found in 45 patients (39%). Patients with the diagnosis of SLE or otherimmune diseases showed the highest positivity (56%) whereas those with thromboembolism, recurrent abortion etc. were only positive in 27%.Among these 45 positive patients the TTI was positive in 41 cases (91 %);however in 10 cases (24 %) this was the only positivity found. The KCT test and the APTT dilution test were both positive in 18 cases (40 %). Anti-cardiolipin antibodies were found in 21 patients (47 %): IgG only in 12 (27 %), IgM only in 5 (11 %), both IgG and IgM in 2 (4 %); in 19 of these 21 patientsthe TTI was also positive.In our study the TTI test seems to be the most sensitive test but possibly also the test with the highest aspecific positivities. IgG and IgM anti-cardiolipin antibodies were less frequently found than expected.
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Fujikawa, K., T. Funakoshi, R. L. Heimark, and J. F. Tait. "HUMAN PLACENTAL ANTICOAGULANT PROTEIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642949.
Abstract:
Endothelium is important to maintain blood fluidity preventing coagulation. Glycosaminoglycan in the endothelial cell plasma membrane has been thought to prevent activation of blood coagulation. Heparin-like compound, which is a potent anticoagulant activity, has been localized on the surface of the cultured endothelial cells. Anticoagulant action associated with thrombomodulin, which is present in endothelial cells, is another mechanism to provide hemostatic nature of endothelial cells.We wondered whether any other intracellular protein(s) is involved in coagulation. We looked for such a protein(s) in cultured bovine aortic endothelial cells. We soon found an anticoagulant activity in the soluble fraction of endothelial cells and it was partially purified. This activity was adsorbed to DEAE-Sepharose and eluted from a gel filtration column in a molecular weight range of 30,000-40,000. However, limited amounts of the cells made it difficult to purify this activity. We then chose human placenta as a substitute source of this protein and have continued the purification of this anticoagulant activity.In this communication, we describe the isolation and characterization of a placental anticoagulant protein, called "PAP", which is silmilar or possible same as the endothelial anticoaguant protein. PAP was purified from the soluble fraction of human placenta by ammonium sulfate precipitation and column chromatography on DEAE-Sepharose, Sephadex G-75, and mono S (Pharmacia). Approximately 20 mg of the protein was purified from one placenta. The purified protein gave a single band by SDS polyacrylamide gel electrophoresis with a molecular weight of 36,500. This protein inhibited both kaolin- and thromboplastin-induced partial thromboplastin times of normal human plasma. It also inhibited the clotting time of platelet-rich plasma induced by factor Xa, but did not affect the thrombin activity of fibrinogen-fibrin conversion. The purified protein completely inhibited the prothrombin activation by reconstituted prothrombinase. The protein neither inhibited the amidolytic activity of factor Xa nor bound factor Xa. This protein specifically bound to phospholipid vesicles (20% phosphatidylserine and 80% phosphatidylcholine) in the presence of calcium ions. These results indicate that PAP inhibits coagulation through the binding to phospholipid vesicles. The study on the amino acid sequence of PAP is in progress in our laboratory. Surprisingly, the sequence analysis of the cyanogen bromide fragments revealed that PAP is a new member of the lipocortin or calpactin family. The sequences of several cyanogen bromide fragments of PAP aligns with the sequences of lipocortin I and II with over 50% identity.Since PAP interacts directly with phospholipid rather than factor Xa, other activation steps in the coagulation cascade, in which phospholipid is involved, are pro^|bly affected by PAP. These reactions are the activation of factor X by a complex of factor IXa-factor VIIIa-phospholipid-Ca++ and the activations of factor X and factor IX by a tissue factor-factor VIIa-Ca++ complex.Reutelingsperger et. al,, have reported the isolation of a novel inhibitor from arteries of human umbilical cord. This protein inhibited the prothrombin activation by prothrombinase. The authors proposed that the inhibition mechanism of this inhibitor was a competition with factor Xa for binding to phospholipid. This protein is very similar to PAP as to the mode of inhibition. The molecular weight of this inhibitor is 32,000, which is slightly smaller than PAP. With the limited chemical characterization of this protein, presently it is difficult to identify this inhibitor with PAP.At the present time, the physiological role and origin of PAP is not known. PAP may originate from the endothelium of placenta, because we have detected a PAP-like anticoagulant activity in bovine aortic endothelial cells. This activity and PAP were quite alike in the purification up to the gel filtration step. If PAP antibody recognizes the antigen in the endothelial cells, it is interesting to see whether PAP localizes on the surface or inside the cells. Nevertheless, if PAP is present in the endothelial cells, it may play an important role to maintain the hemostatic nature of endothelium. PAP may bind phospholipid components at injured sites, before coagulation factors come in contact with lipid components and initiate thrombolytic events.
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Gordon, Stuart, Bonnie Sloane, Phil Cavanugh, Barbara Cross, Kenneth Honn, and Mohanathasan Chelladurai. "PURIFICATION AND CHARACTERIZATION OF TWO PROCOAGULANTS FROM WALKER 256 CARCINOSARCOMA TUMORS,." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643666.
Abstract:
Activation of the coagulation system bytumor cells may play an important role in tumor growth and metastases. Becauseprocoagulant activities have been identified in different tumor cells by different investigators, effective comparison of these activities has been difficult. Therefore, we purified and characterized two different procoagulant proteins from the same Walker 256 tumors. The first procoagulant activity/platelet aggregating activity (PCA/PAA) was purified from a 1% CHAPS detergent extract oftumor homogenate followed by (NH4)2SO4 fractionation, anion exchange and hydrophobic chromatography. The protein had a molecular weight of 58,000, required phospholipid and an intact coagulation pathway from factor X through fibrinogen for activity, but did not require factors VII or IX forits procoagulant activity. The procoagulant activity was not inhibited by 5mMphenyl-methyl sulfonyl fluoride, iodoacetamide or phenanthroline; there was noevidence of proteinase activity. The PAA was due to thrombin generation during coagulation. The second procoagulant,cancer procoagulant (CP), was extracted from tumors in barbital buffer (pH 7.4) without detergent, purified by immunoaffinity (using a polyclonal goat antibody to CP from V2 carcinoma) and mercurial-benzoate affinity chromatography. CP had a molecular weight of 68,000, an isoelectric point of 4.8 and initiated coagulation by directly activating factor X in the coagulation system. CP was inhibited by Hg++ and iodoacetamide, cysteine proteinase inhibitors. The purified CP formed an immunodiffusion precipitin band against the polyclonal anti-CP goat antibody. Thus, thepurified CP had the same physicochemical, enzymatic and immunologic propertiesas CP from rabbit V2 carcinoma. Neither procoagulant had the properties of tissue factor. These results suggest that there aretwo distinct procoagulant activities inWalker 256 and that both may contributeto the coagulation abnormalities that are associated with tumor growthand metastases.