Search results for "c1q"

showing 10 items of 60 documents

Subcellular targeting of multiligand-binding protein gC1qR.

1999

Abstract gC1q receptor, a protein originally described as the cell surface receptor for the globular heads of complement factor C1q, has been found to bind human H-kininogen with high affinity and specificity. Therefore, gC1qR has been considered candidate kininogen docking site on the surfaces of platelets, neutrophils and endothelial cells. Recent work demonstrating that gC1qR is an intracellular protein that is tightly associated with mitochondria rather than targeted to the cell surface has challenged this view. To further probe cellular trafficking routes of gC1qR, we overexpressed human gC1qR in a mammalian cell and monitored cell surface exposure of recombinant gC1qR by virtue of its…

CellComplement factor IBiologyLigandsMitochondrial ProteinsCell surface receptormedicineAnimalsHumansBinding siteReceptorPharmacologyBinding SitesMembrane GlycoproteinsBinding proteinComplement C1qBiological TransportTransfectionMolecular biologyCell biologyReceptors Complementmedicine.anatomical_structureHyaluronan ReceptorsCell cultureCOS CellsCarrier ProteinsProtein Processing Post-Translationalcirculatory and respiratory physiologySubcellular FractionsImmunopharmacology
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Expression of C1q, a subcomponent of the rat complement system, is dramatically enhanced in brains of rats with either Borna disease or experimental …

1995

In situ hybridization, RT-PCR and Northern blot analysis as well immunohistochemistry were used to examine the expression of C1q, a subcomponent of the rat complement system, in brains of rats infected with Borna disease virus (BDV) and rats afflicted with experimental allergic encephalomyelitis (EAE) induced by the adoptive transfer of myelin basic protein specific T cells. C1q mRNA, which was not detected in normal brain, became clearly detectable using RT-PCR analysis by d14 post infection (p.i.) with BDV. Maximal levels of C1q mRNA were reached 21 days p.i. when inflammatory reactions in the brain were also at a peak. Similarly, C1q mRNA was elevated when the clinical symptoms of EAE be…

Pathologymedicine.medical_specialtyAdoptive cell transferEncephalomyelitis Autoimmune ExperimentalEncephalomyelitisMolecular Sequence Datachemical and pharmacologic phenomenaIn situ hybridizationBiologyHippocampusPolymerase Chain Reactionimmune system diseasesGlial Fibrillary Acidic ProteinmedicineAnimalsNorthern blotRNA MessengerIn Situ HybridizationBrain ChemistryBorna diseaseMicrogliaBase SequenceComplement C1qRNA-Directed DNA Polymerasemedicine.diseaseBlotting NorthernImmunohistochemistryMyelin basic proteinComplement systemRatsUp-RegulationBlotting Southernmedicine.anatomical_structureNeurologyBorna Diseasebiology.proteinFemaleNeurology (clinical)MicrogliaJournal of the neurological sciences
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Complement C1q and C8beta deficiency in an individual with recurrent bacterial meningitis and adult-onset systemic lupus erythematosus-like illness.

2008

Co-existing complement C8 deficiency ameliorated the SLE associated with C1q deficiency.

Lupus erythematosusLupus Erythematosusbusiness.industryComplementmedicine.diseaseLupus ErythematosuRheumatologyBacterial MeningitisImmunologymedicinePharmacology (medical)Bacterial meningitisComplement; Lupus Erythematosus; Bacterial MeningitisRecurrent bacterial meningitisbusinessMeningitisComplement C1qAnti-SSA/Ro autoantibodies
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Binding to complement factors and activation of the alternative pathway by Acanthamoeba.

2010

Acanthamoeba can cause severe ocular and cerebral diseases in healthy and immunocompromised individuals, respectively. Activation of complement appears to play an important role in host defence against infection. The exact mechanism, however, is still unclear. The aim of the present study was to investigate the effect of normal human serum (NHS) and normal mouse serum (NMS) on Acanthamoeba trophozoites, the binding of different complement factors to Acanthamoeba and the activation of the complement system. Moreover, we aimed to work out any possible differences between different strains of Acanthamoeba. A virulent T4 strain, a non-virulent T4 strain and a virulent T6 strain were included in…

ImmunologyComplement Pathway AlternativeVirulenceAcanthamoebaComplement factor IAntigen-Antibody ComplexImmunofluorescenceMannose-Binding LectinBacterial AdhesionMicrobiologyMiceSpecies Specificityparasitic diseasesmedicineImmunology and AllergyAnimalsHumansTrophozoitesIncubationEdetic AcidMice Knockoutmedicine.diagnostic_testbiologyVirulenceComplement C1qHematologyAmebiasisComplement C3biology.organism_classificationComplement C9Complement systemAcanthamoebaMice Inbred C57BLAlternative complement pathwayIntracellularImmunobiology
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Modulation of C1q mRNA Expression and Secretion by Interleukin-1,Interleukin-6, and Interferon-g in Resident and Stimulated Murine Peritoneal Macroph…

2002

The complement system plays an important role in the humoral immune response. Activation of the classical complement pathway is mediated by its subcomponent, C1q. Among the main C1q-synthesising tissues, macrophages have been attributed as a source of particular importance. We investigated the effects of cytokines (IL-1, IL-6 and Interferon-gamma) on local C1q mRNA expression and C1q secretion in resident and in thioglycollate-stimulated murine peritoneal macrophages in vitro. The macrophages were isolated from murine peritoneal lavage fluid, maintained in culture and incubated with the cytokines. Among the cytokines, only IL-6 had a stimulatory effect on C1q production (25% increase vs. co…

ImmunologyGene Expressionchemical and pharmacologic phenomenaIn Vitro TechniquesProinflammatory cytokineInterferon-gammaMiceClassical complement pathwayImmune systemmedicineAnimalsImmunology and AllergyMacrophageInterferon gammaRNA MessengerInterleukin 6Macrophage inflammatory proteinMice Inbred BALB CbiologyInterleukin-6ChemistryComplement C1qInterleukinHematologyMacrophage ActivationRecombinant ProteinsCell biologyThioglycolatesMacrophages Peritonealbiology.proteinInterleukin-1medicine.drugImmunobiology
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Anti-C1q Autoantibodies in Lupus Nephritis: Prevalence and Clinical Significance

2005

Recently, anti-C1q autoantibodies have been proposed as a useful marker in systemic lupus erythematosus (SLE) since their occurrence correlates with renal involvement and, possibly, with nephritic activity. We aimed to evaluate the prevalence of anti-C1q antibodies in patients with SLE, with and without renal involvement, and to correlate these markers' presence and levels with the activity of the disease and nephropathy. We studied 61 patients with SLE, 40 of whom had biopsy-proven lupus nephritis; 35 patients with other connective tissue diseases; and 54 healthy controls. In addition, 18 lupus nephritis patients were followed up during the disease time course. Anti-C1q antibodies were mea…

BiopsySLELupus nephritisEnzyme-Linked Immunosorbent AssaySystemic lupus erythematosuAnti-DNA antibodieSeverity of Illness IndexGeneral Biochemistry Genetics and Molecular BiologyFollow-Up StudieNephropathyCohort StudiesHistory and Philosophy of Scienceimmune system diseasesAutoimmune diseasePrevalencemedicineHumansLupus Erythematosus SystemicConnective Tissue DiseasesGlomerulonephritiskin and connective tissue diseasesRenal flareConnective Tissue DiseaseAutoantibodiesAutoimmune diseaseBiochemistry Genetics and Molecular Biology (all)Systemic lupus erythematosusbusiness.industryLupus nephritiComplement C1qGeneral NeuroscienceAutoantibodyGlomerulonephritisBiomarkermedicine.diseaseLupus NephritisAutoantibodieAntibodies Anti-IdiotypicItalyAntibodies AntinuclearImmunologyAnti-C1q antibodieCohort StudiebusinessNephritisBiomarkersFollow-Up StudiesHumanAnti-SSA/Ro autoantibodiesAnnals of the New York Academy of Sciences
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C1q as a novel player in angiogenesis with therapeutic implication in wound healing

2014

We have previously shown that C1q is expressed on endothelial cells (ECs) of newly formed decidual tissue. Here we demonstrate that C1q is deposited in wound-healing skin in the absence of C4 and C3 and that C1q mRNA is locally expressed as revealed by real-time PCR and in situ hybridization. C1q was found to induce permeability of the EC monolayer, to stimulate EC proliferation and migration, and to promote tube formation and sprouting of new vessels in a rat aortic ring assay. Using a murine model of wound healing we observed that vessel formation was defective in C1qa(-/-) mice and was restored to normal after local application of C1q. The mean vessel density of wound-healing tissue and …

Pathologymedicine.medical_specialtycomplement C1qAngiogenesisImmunoblottingNeovascularization Physiologicchemical and pharmacologic phenomenaEnzyme-Linked Immunosorbent AssayIn situ hybridizationBiologyReal-Time Polymerase Chain ReactionangiogenesisMiceVasculogenesiscomplement; vasculogenesis; animal modelsimmune system diseasesmedicineangiogenesis; complement C1q; wound-healing; endothelial cellsHuman Umbilical Vein Endothelial CellsAnimalsHumanscomplementRats WistarIn Situ HybridizationCell ProliferationDNA PrimersTube formationMice KnockoutWound HealingMultidisciplinaryCell growthComplement C1qEndothelial CellsangiogenesivasculogenesiBiological Scienceswound-healingImmunohistochemistryanimal modelsendothelial cellsRatsMice Inbred C57BLReal-time polymerase chain reactionImmunohistochemistryWound healing
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The role of accessory cells in polyclonal T cell activation. I. Both induction of interleukin 2 production and of interleukin 2 responsiveness by con…

1983

Recent studies from other laboratories have shown that concanavalin A (Con A) acts at two separate steps in polyclonal T cell activation: interleukin 2 (IL2) production, and induction of responsiveness to IL2. Using a combination of techniques for the depletion of accessory cells from lymph node T cells, we have investigated which of these steps, if not both, is responsible for the known requirement for accessory cells in the Con A response. It was found that with increasing T cell purification, first the ability is lost to produce sufficient levels of endogenous IL2, whereas induction of IL2 responsiveness can still take place. Further removal of accessory cells however yields a population…

Malemusculoskeletal diseasesInterleukin 2medicine.medical_specialtyComplement Activating EnzymesT-LymphocytesT cellLymphocyte CooperationImmunologyPopulationchemical and pharmacologic phenomenaLymphocyte ActivationMiceInterleukin 21immune system diseasesInternal medicineConcanavalin AmedicineAnimalsImmunology and AllergyAntigen-presenting celleducationInterleukin 3LymphokinesMice Inbred BALB Ceducation.field_of_studybiologyComplement C1qImmune SeraHistocompatibility Antigens Class IIhemic and immune systemsCell biologyKineticsstomatognathic diseasesEndocrinologymedicine.anatomical_structurePolyclonal antibodiesConcanavalin Abiology.proteinInterleukin-2FemaleLymph NodesSpleenmedicine.drugEuropean Journal of Immunology
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Distinct Roles of Classical and Lectin Pathways of Complement in Preeclamptic Placentae

2022

Pre-eclampsia is a pregnancy complication characterized by defective vascular remodeling in maternal decidua responsible for reduced blood flow leading to functional and structural alterations in the placenta. We have investigated the contribution of the complement system to decidual vascular changes and showed that trophoblasts surrounding unremodeled vessels prevalent in preeclamptic decidua fail to express C1q that are clearly detected in cells around remodeled vessels predominant in control placenta. The critical role of C1q is supported by the finding that decidual trophoblasts of femaleC1qa-/-pregnant mice mated toC1qa+/+male mice surrounding remodeled vessels express C1q of paternal …

Malepre-eclampsiavascular remodelingComplement System ProteinPlacentaImmunologyMannose-Binding Protein-Associated Serine ProteaseSettore MED/08 - Anatomia PatologicaPre-Eclampsia.MicePregnancyLectinsficolin-3Immunology and AllergyAnimalsHumansSettore MED/05 - Patologia Clinicacomplement system; pre-eclampsia; vascular remodeling; C1q; ficolin-3C1qcomplement systemAnimalComplement C1qEndothelial CellsComplement System ProteinsMannose-Binding Protein-Associated Serine ProteasesFemale
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C1q induces in vivo angiogenesis and promotes wound healing

2011

C1q; angiogenesisangiogenesisChemistryAngiogenesisIn vivoImmunologyCancer researchSettore MED/08 - Anatomia PatologicaWound healingMolecular BiologyC1q
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