The Experts below are selected from a list of 48243 Experts worldwide ranked by ideXlab platform
Berhane Ghebrehiwet - One of the best experts on this subject based on the ideXlab platform.
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Complement Activation on platelets: implications for vascular inflammation and thrombosis.
Molecular immunology, 2010Co-Authors: Ellinor I.b. Peerschke, Wei Yin, Berhane GhebrehiwetAbstract:Platelets participate in a variety of responses of the blood to injury. An emerging body of evidence suggests that these cells express an intrinsic capacity to interact with and trigger both classical and alternative pathways of Complement. This activity requires cell Activation with biochemical agonists and/or shear stress, and is associated with the expression of P-selectin, gC1qR, and chondroitin sulfate. Platelet mediated Complement Activation measurably increases soluble inflammatory mediators (C3a and C5a). Platelets may also serve as targets of classical Complement Activation in autoimmune conditions such as antiphospholipid syndromes (APS) and immune thrombocytopenia purpura (ITP). Retrospective correlation with clinical data suggests that enhanced platelet associated Complement Activation correlates with increased arterial thrombotic events in patients with lupus erythematosus and APS, and evidence of enhanced platelet clearance from the circulation in patients with ITP. Taken together, these data support a role for platelet mediated Complement Activation in vascular inflammation and thrombosis.
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Platelet mediated Complement Activation.
Advances in experimental medicine and biology, 2008Co-Authors: Ellinor I.b. Peerschke, Wei Yin, Berhane GhebrehiwetAbstract:The Complement system comprises a series of proteases and inhibitors that are activated in cascade-like fashion during host defense (Makrides 1998). A growing body of evidence supports the hypothesis that immune mechanisms, including Complement Activation, are involved in inflammatory conditions associated with vascular injury (Acostan et al. 2004; Giannakopoulos et al. 2007), and disseminated intravascular coagulation associated with massive trauma (Huber-Lang, this volume). We propose that platelets and platelet derived microparticles focus Complement to sites of vascular injury where regulated Complement Activation participates in clearing terminally activated platelets and microparticles from the circulation, and dysregulated Complement Activation contributes to inflammation and thrombosis. Given the central role of platelets in hemostasis and thrombosis, it is not surprising that activated Complement components have been demonstrated in many types of atherosclerotic and thrombotic vascular lesions (Torzewsjki et al. 2007; Niculescu et al. 2004).
Ellinor I.b. Peerschke - One of the best experts on this subject based on the ideXlab platform.
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Complement Activation on platelets: implications for vascular inflammation and thrombosis.
Molecular immunology, 2010Co-Authors: Ellinor I.b. Peerschke, Wei Yin, Berhane GhebrehiwetAbstract:Platelets participate in a variety of responses of the blood to injury. An emerging body of evidence suggests that these cells express an intrinsic capacity to interact with and trigger both classical and alternative pathways of Complement. This activity requires cell Activation with biochemical agonists and/or shear stress, and is associated with the expression of P-selectin, gC1qR, and chondroitin sulfate. Platelet mediated Complement Activation measurably increases soluble inflammatory mediators (C3a and C5a). Platelets may also serve as targets of classical Complement Activation in autoimmune conditions such as antiphospholipid syndromes (APS) and immune thrombocytopenia purpura (ITP). Retrospective correlation with clinical data suggests that enhanced platelet associated Complement Activation correlates with increased arterial thrombotic events in patients with lupus erythematosus and APS, and evidence of enhanced platelet clearance from the circulation in patients with ITP. Taken together, these data support a role for platelet mediated Complement Activation in vascular inflammation and thrombosis.
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Platelet mediated Complement Activation.
Advances in experimental medicine and biology, 2008Co-Authors: Ellinor I.b. Peerschke, Wei Yin, Berhane GhebrehiwetAbstract:The Complement system comprises a series of proteases and inhibitors that are activated in cascade-like fashion during host defense (Makrides 1998). A growing body of evidence supports the hypothesis that immune mechanisms, including Complement Activation, are involved in inflammatory conditions associated with vascular injury (Acostan et al. 2004; Giannakopoulos et al. 2007), and disseminated intravascular coagulation associated with massive trauma (Huber-Lang, this volume). We propose that platelets and platelet derived microparticles focus Complement to sites of vascular injury where regulated Complement Activation participates in clearing terminally activated platelets and microparticles from the circulation, and dysregulated Complement Activation contributes to inflammation and thrombosis. Given the central role of platelets in hemostasis and thrombosis, it is not surprising that activated Complement components have been demonstrated in many types of atherosclerotic and thrombotic vascular lesions (Torzewsjki et al. 2007; Niculescu et al. 2004).
Marina A. Dobrovolskaia - One of the best experts on this subject based on the ideXlab platform.
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Analysis of Complement Activation by Nanoparticles.
Methods in molecular biology (Clifton N.J.), 2017Co-Authors: Barry W. Neun, Anna N. Ilinskaya, Marina A. DobrovolskaiaAbstract:The Complement system is a group of proteins, which function in plasma to assist the innate immunity in rapid clearance of pathogens. The Complement system also contributes to coordination of the adaptive immune response. Complement Activation Related Pseudo Allergy or CARPA is a life-threatening condition commonly reported with certain types of drugs and nanotechnology-based combination products. While CARPA symptoms are similar to that of anaphylaxis, the mechanism behind this pathology does not involve IgE and is mediated by the Complement system. In vitro assays using serum or plasma derived from healthy donor volunteers correlate with the in vivo Complement-mediated reactions, and therefore are helpful in understanding the propensity of a given drug formulation to cause CARPA in patients. In the first edition of this book, we have described an in vitro method for qualitative assessment of the Complement Activation by nanomaterials using western blotting. Herein, we present a similar method utilizing enzyme-linked immunoassay for quantitative analysis of the Complement Activation, and we compare the performance of this approach to that of the qualitative western blotting technique. The revised chapter also includes new details about nanoparticle sample preparation.
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Qualitative Analysis of Total Complement Activation by Nanoparticles
Methods in molecular biology (Clifton N.J.), 2010Co-Authors: Barry W. Neun, Marina A. DobrovolskaiaAbstract:This chapter describes a method for qualitative detection of Complement Activation by western blot. This method uses the cleavage product of the C3 component as a marker for Complement Activation by any pathway. In this protocol, human plasma is exposed to nanoparticles and then analyzed by polyacrylamide gel electrophoresis (PAGE) followed by western blot with anti-C3-specific antibodies. These antibodies recognize both the native C3 component of Complement and its cleavage products. The amounts of C3 and the C3 cleavage products are compared to the amounts in control (untreated) plasma and to plasma treated with a positive control to provide a quick and inexpensive qualitative assessment of Complement Activation.
Wei Yin - One of the best experts on this subject based on the ideXlab platform.
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Complement Activation on platelets: implications for vascular inflammation and thrombosis.
Molecular immunology, 2010Co-Authors: Ellinor I.b. Peerschke, Wei Yin, Berhane GhebrehiwetAbstract:Platelets participate in a variety of responses of the blood to injury. An emerging body of evidence suggests that these cells express an intrinsic capacity to interact with and trigger both classical and alternative pathways of Complement. This activity requires cell Activation with biochemical agonists and/or shear stress, and is associated with the expression of P-selectin, gC1qR, and chondroitin sulfate. Platelet mediated Complement Activation measurably increases soluble inflammatory mediators (C3a and C5a). Platelets may also serve as targets of classical Complement Activation in autoimmune conditions such as antiphospholipid syndromes (APS) and immune thrombocytopenia purpura (ITP). Retrospective correlation with clinical data suggests that enhanced platelet associated Complement Activation correlates with increased arterial thrombotic events in patients with lupus erythematosus and APS, and evidence of enhanced platelet clearance from the circulation in patients with ITP. Taken together, these data support a role for platelet mediated Complement Activation in vascular inflammation and thrombosis.
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Platelet mediated Complement Activation.
Advances in experimental medicine and biology, 2008Co-Authors: Ellinor I.b. Peerschke, Wei Yin, Berhane GhebrehiwetAbstract:The Complement system comprises a series of proteases and inhibitors that are activated in cascade-like fashion during host defense (Makrides 1998). A growing body of evidence supports the hypothesis that immune mechanisms, including Complement Activation, are involved in inflammatory conditions associated with vascular injury (Acostan et al. 2004; Giannakopoulos et al. 2007), and disseminated intravascular coagulation associated with massive trauma (Huber-Lang, this volume). We propose that platelets and platelet derived microparticles focus Complement to sites of vascular injury where regulated Complement Activation participates in clearing terminally activated platelets and microparticles from the circulation, and dysregulated Complement Activation contributes to inflammation and thrombosis. Given the central role of platelets in hemostasis and thrombosis, it is not surprising that activated Complement components have been demonstrated in many types of atherosclerotic and thrombotic vascular lesions (Torzewsjki et al. 2007; Niculescu et al. 2004).
Bo Nilsson - One of the best experts on this subject based on the ideXlab platform.
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Properdin in Complement Activation and Tissue Injury
Molecular immunology, 2013Co-Authors: Allison M. Lesher, Bo Nilsson, Wen-chao SongAbstract:The plasma protein properdin is the only known positive regulator of Complement Activation. Although regarded as an initiator of the alternative pathway of Complement Activation at the time of its discovery more than a half century ago, the role and mechanism of action of properdin in the Complement cascade has undergone significant conceptual evolution since then. Despite the long history of research on properdin, however, new insight and unexpected findings on the role of properdin in Complement Activation, pathogen infection and host tissue injury are still being revealed by ongoing investigations. In this article, we provide a brief review on recent studies that shed new light on properdin biology, focusing on the following three topics: (1) its role as a pattern recognition molecule to direct and trigger Complement Activation, (2) its context-dependent requirement in Complement Activation on foreign and host cell surfaces, and (3) its involvement in alternative pathway Complement-mediated immune disorders and considerations of properdin as a potential therapeutic target in human diseases.
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binding of a model regulator of Complement Activation rca to a biomaterial surface surface bound factor h inhibits Complement Activation
Biomaterials, 2001Co-Authors: Jonas Andersson, Rolf Larsson, R Richter, Kristina Nilsson Ekdahl, Bo NilssonAbstract:The Complement system is an important inflammatory mediator during procedures such as cardiopulmonary bypass and hemodialysis when blood is exposed to large areas of biomaterial surface. This contact between blood and the biomaterials of implants and extracorporeal circuits leads to an inflammatory response mediated by the Complement system. The aim of this study was to assess the ability of a Complement regulator (factor H) immobilised on a biomaterial surface to inhibit Complement cascade mediated inflammatory responses. The cross-linker N-succinimidyl 3-(2-pyridyldithio) propionate was used to immobilise factor H on a model biomaterial surface without affecting the biological activity of the inhibitor. Binding of factor H was then characterised using quartz crystal microbalance-dissipation (QCM-D) and enzyme immunoassays for products of Complement Activation: bound C3 fragments and soluble C3a, sC5b-9, and C1s-C1INA. Immobilised factor H reduced the amount C3 fragments deposited on the biomaterial surface after incubation with serum, plasma, or whole blood. In addition, lower levels of soluble C3a and sC5b-9 were generated after incubation with whole blood. In summary, we have demonstrated that Complement Activation on a highly activating model surface can be inhibited by immobilised factor H and have defined prerequisites for the preparation of future biomaterial surfaces with immobilised regulators of Complement Activation.