Search results for "Complement system"
showing 10 items of 157 documents
Complement Protein C1q Binds to Hyaluronic Acid in the Malignant Pleural Mesothelioma Microenvironment and Promotes Tumor Growth
2017
C1q is the first recognition subcomponent of the complement classical pathway, which acts towards the clearance of pathogens and apoptotic cells. C1q is also known to modulate a range of functions of immune and non-immune cells, including their involvement in placental development and sensorial synaptic pruning. We have recently shown that C1q can promote tumour by encouraging their adhesion, migration and proliferation in addition to angiogenesis and metastasis. In this study, we have examined the role of C1q in the microenvironment of malignant pleuric mesothelioma (MPM), a rare form of cancer commonly associated with exposure to asbestos. We found that C1q was highly expressed in all MPM…
Pathogenic Role of Complement in Antiphospholipid Syndrome and Therapeutic Implications
2018
Antiphospholipid syndrome (APS) is an acquired autoimmune disease characterized by thromboembolic events, pregnancy morbidity, and the presence of antiphospholipid (aPL) antibodies. There is sound evidence that aPL act as pathogenic autoantibodies being responsible for vascular clots and miscarriages. However, the exact mechanisms involved in the clinical manifestations of the syndrome are still a matter of investigation. In particular, while vascular thrombosis is apparently not associated with inflammation, the pathogenesis of miscarriages can be explained only in part by the aPL-mediated hypercoagulable state and additional non-thrombotic effects, including placental inflammation, have b…
Is the Complement Protein C1q a Pro- or Anti-tumorigenic Factor? Bioinformatics Analysis Involving Human Carcinomas
2019
C1q is the first subcomponent of the classical pathway of the complement system and belongs to the C1q/Tumor Necrosis Factor superfamily. C1q can perform a diverse range of immune and non-immune functions in a complement-dependent as well as -independent manner. Being a pattern recognition molecule of the innate immunity, C1q can recognize a number of self, non-self and altered-self ligands and bring about effector mechanisms designed to clear pathogens via opsonisation and inflammatory response. C1q is locally synthesized by macrophages and dendritic cells, and thus, can get involved in a range of biological processes, such as angiogenesis and tissue remodeling, immune modulation, and immu…
Analysis of complement C3 activation products in human atherosclerotic lesions.
1991
Abstract Cleavage of the complement C3 protein is essential for complement activation. Saline extracts of human atherosclerotic lesions were examined by various techniques for the presence of C3 cleavage fragments. Crossed intermediate gel immunoelectrophoresis revealed that native C3 was the predominate C3 protein in extracts and that the C3dg fragment was also detected. SDS-PAGE/ Western blot analyses of lesion extracts employing monoclonal antibodies directed at C3c and C3dg fragment determinants demonstrated molecular weight bands corresponding to the known molecular weights of all the physiologic C3 cleavage fragments, except Cab which is known to have a short half-life. After C3, the …
Monoclonal antibodies against components of the classical pathway of complement.
1989
Activation of the classical pathway of complement involves several binding and enzymatic cleavage processes. Binding and enzymatic activation results in the appearance of new structures in the individual components. This report describes the different activation steps for C1q, C1r, C1s, C4 and C2 and summarizes monoclonal antibodies reported so far which recognize either conserved epitopes or activation-dependent epitopes with particular emphasis on neoepitopes occurring during the activation cascade.
Is cell salvage safe in liver resection? A pilot study
2007
Abstract Study Objective To investigate the quality of cell salvaged (CS) blood in patients undergoing hemihepatectomy (study group) and compare it with CS-blood from aortic surgery (control group). Design Observational study. Setting Operating room in a university hospital. Measurements 6 patients undergoing hemihepatectomy or aortobifemoral bypass with intraoperative blood loss of more than 800 mL. Samples were drawn from the central venous catheter, from the reservoir of a CS recovery system, and from the processed blood in each patient to determine interleukin (IL)-6, IL-8, IL-10, tumor necrosis factor (TNF), complement C3a, and the terminal complement complex C5b-9. Microbiological ana…
Decidual endothelial cells express surface-bound C1q as a molecular bridge between endovascular trophoblast and decidual endothelium.
2008
This study was prompted by the observation that decidual endothelial cells (DECs), unlike endothelial cells (ECs) of blood vessels in normal skin, kidney glomeruli and brain, express surface-bound C1q in physiologic pregnancy. This finding was unexpected, because deposits of C1q are usually observed in pathologic conditions and are associated with complement activation. In the case of DECs, we failed to detect immunoglobulins and C4 co-localized with C1q on the cell surface. Surprisingly, DECs expressed mRNA for the three chains of C1q and secreted detectable level of this component in serum-free medium. The ability to synthesize C1q is acquired by DECs during pregnancy and is not shared by…
Complement activation by oxidatively modified low-density lipoproteins
1999
Background Oxidatively modified low-density lipoproteins (LDLs) have been implicated in the pathogenesis of atherosclerosis and are found in human vascular lesions. There is increasing evidence that complement activation may also play a role in atherogenesis. Activated complement proteins have been demonstrated to be present in early atherosclerotic lesions, and lipids isolated from lesions have been shown to activate complement, hence their designation as lesion complement activator (LCA). The question now arose whether oxidized LDLs would also activate complement. Material and methods The complement-activating capacity of a lesion complement activator preparation and of minimally as well …
Complement C6 deficiency protects against diet-induced atherosclerosis in rabbits.
1998
Abstract —Low-density lipoprotein (LDL) can be transformed to an atherogenic moiety by nonoxidative, enzymatic degradation. Enzymatically degraded LDL induces macrophage foam cell formation, provokes release of cytokines, and also activates complement. To determine whether complement activation may contribute to atherogenesis, 6 pairs of homozygous C6-deficient rabbits and their non–C6-deficient heterozygous siblings were fed a cholesterol-rich diet for 14 weeks. Cholesterol levels and plasma lipoprotein profiles of the animals in the C6-competent and C6-deficient groups did not significantly differ, and the high density lipoprotein and LDL cholesterol ratios at the end of the experiment w…
Hereditary angioneurotic oedema and blood-coagulation: interaction between C1-esterase-inhibitor and the activation factors of the proteolytic enzyme…
1983
C-1-inactivator (C-1-INA) does not only exert its important inhibitory functions in the complement system but also in the first step in the activation of the coagulation, fibrinolytic and kallikrein system. We therefore determined in nine patients with hereditary angioneurotic oedema (HANE) with obvious quantitative or functional defects of C-1-INA, and one further patient with Quincke-type oedema of different origin, the coagulation factors of the initial phase such as Hageman factor, plasma thromboplastin antecedent (PTA) and high molecular weight kininogen (HMWK). These factors were further correlated with the concentration as well as functional activity of C-1-INA. Nine of ten patients …