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[PMID]:27077104
[Au] Autor:Leung LL; Morser J
[Ad] Endereço:Stanford University School of Medicine, Division of Hematology, Stanford, CA 94305, USA.
[Ti] Título:Plasmin as a complement C5 convertase.
[So] Source:EBioMedicine;5:20-1, 2016 Mar.
[Is] ISSN:2352-3964
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Mh] Termos MeSH primário: Convertases de Complemento C3-C5
Fibrinolisina
[Mh] Termos MeSH secundário: Enzimas Ativadoras do Complemento
Ativação do Complemento
Complemento C2
Complemento C3
Complemento C3b
Complemento C4
Complemento C5
Complemento C6
Complemento C9
Via Alternativa do Complemento
Seres Humanos
[Pt] Tipo de publicação:COMMENT; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Complement C2); 0 (Complement C3); 0 (Complement C4); 0 (Complement C5); 0 (Complement C6); 0 (Complement C9); 80295-43-8 (Complement C3b); EC 3.- (Complement Activating Enzymes); EC 3.4.21.- (Complement C3-C5 Convertases); EC 3.4.21.7 (Fibrinolysin)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:160416
[Lr] Data última revisão:
160416
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160415
[St] Status:MEDLINE
[do] DOI:10.1016/j.ebiom.2016.03.015


  2 / 1273 MEDLINE  
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[PMID]:26517887
[Au] Autor:Makou E; Herbert AP; Barlow PN
[Ad] Endereço:School of Chemistry, The University of Edinburgh, Joseph Black Building, David Brewster Road, Edinburgh EH9 3FJ, U.K.
[Ti] Título:Creating functional sophistication from simple protein building blocks, exemplified by factor H and the regulators of complement activation.
[So] Source:Biochem Soc Trans;43(5):812-8, 2015 Oct.
[Is] ISSN:1470-8752
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Complement control protein modules (CCPs) occur in numerous functionally diverse extracellular proteins. Also known as short consensus repeats (SCRs) or sushi domains each CCP contains approximately 60 amino acid residues, including four consensus cysteines participating in two disulfide bonds. Varying in length and sequence, CCPs adopt a ß-sandwich type fold and have an overall prolate spheroidal shape with N- and C-termini lying close to opposite poles of the long axis. CCP-containing proteins are important as cytokine receptors and in neurotransmission, cell adhesion, blood clotting, extracellular matrix formation, haemoglobin metabolism and development, but CCPs are particularly well represented in the vertebrate complement system. For example, factor H (FH), a key soluble regulator of the alternative pathway of complement activation, is made up entirely from a chain of 20 CCPs joined by short linkers. Collectively, therefore, the 20 CCPs of FH must mediate all its functional capabilities. This is achieved via collaboration and division of labour among these modules. Structural studies have illuminated the dynamic architectures that allow FH and other CCP-rich proteins to perform their biological functions. These are largely the products of a highly varied set of intramolecular interactions between CCPs. The CCP can act as building block, spacer, highly versatile recognition site or dimerization mediator. Tandem CCPs may form composite binding sites or contribute to flexible, rigid or conformationally 'switchable' segments of the parent proteins.
[Mh] Termos MeSH primário: Enzimas Ativadoras do Complemento/química
Ativação do Complemento
Proteínas Inativadoras do Complemento/química
Desenho de Drogas
Modelos Moleculares
Engenharia de Proteínas
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação
Enzimas Ativadoras do Complemento/genética
Enzimas Ativadoras do Complemento/metabolismo
Fator H do Complemento/química
Fator H do Complemento/genética
Fator H do Complemento/metabolismo
Inativadores do Complemento/química
Inativadores do Complemento/metabolismo
Inativadores do Complemento/farmacologia
Proteínas Inativadoras do Complemento/genética
Proteínas Inativadoras do Complemento/metabolismo
Seres Humanos
Fragmentos de Peptídeos/química
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Conformação Proteica
Domínios e Motivos de Interação entre Proteínas
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
Proteínas Recombinantes de Fusão/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Complement Inactivating Agents); 0 (Complement Inactivator Proteins); 0 (Peptide Fragments); 0 (Recombinant Fusion Proteins); 0 (complement factor H, human); 80295-65-4 (Complement Factor H); EC 3.- (Complement Activating Enzymes)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:151031
[Lr] Data última revisão:
151031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151031
[St] Status:MEDLINE
[do] DOI:10.1042/BST20150074


  3 / 1273 MEDLINE  
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[PMID]:24161035
[Au] Autor:Noris M; Remuzzi G
[Ad] Endereço:IRCCS- Istituto di Ricerche Farmacologiche "Mario Negri", Bergamo, Italy. Electronic address: marina.noris@marionegri.it.
[Ti] Título:Overview of complement activation and regulation.
[So] Source:Semin Nephrol;33(6):479-92, 2013 Nov.
[Is] ISSN:1558-4488
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Complement is an important component of the innate immune system that is crucial for defense from microbial infections and for clearance of immune complexes and injured cells. In normal conditions complement is tightly controlled by a number of fluid-phase and cell surface proteins to avoid injury to autologous tissues. When complement is hyperactivated, as occurs in autoimmune diseases or in subjects with dysfunctional regulatory proteins, it drives a severe inflammatory response in numerous organs. The kidney appears to be particularly vulnerable to complement-mediated inflammatory injury. Injury may derive from deposition of circulating active complement fragments in glomeruli, but complement locally produced and activated in the kidney also may have a role. Many kidney disorders have been linked to abnormal complement activation, including immune-complex-mediated glomerulonephritis and rare genetic kidney diseases, but also tubulointerstitial injury associated with progressive proteinuric diseases or ischemia-reperfusion.
[Mh] Termos MeSH primário: Imunidade Adaptativa/fisiologia
Enzimas Ativadoras do Complemento/metabolismo
Ativação do Complemento/fisiologia
Imunidade Inata/fisiologia
Nefropatias/imunologia
[Mh] Termos MeSH secundário: Proteínas do Sistema Complemento
Seres Humanos
Nefropatias/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
9007-36-7 (Complement System Proteins); EC 3.- (Complement Activating Enzymes)
[Em] Mês de entrada:1406
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131029
[St] Status:MEDLINE


  4 / 1273 MEDLINE  
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[PMID]:21664996
[Au] Autor:Degn SE; Jensenius JC; Thiel S
[Ad] Endereço:Department of Medical Microbiology and Immunology, Aarhus University, Wilhelm Meyers Allé 4, 8000 Aarhus C, DK-Denmark. Electronic address: sdegn@microbiology.au.dk.
[Ti] Título:Disease-causing mutations in genes of the complement system.
[So] Source:Am J Hum Genet;88(6):689-705, 2011 Jun 10.
[Is] ISSN:1537-6605
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent studies have revealed profound developmental consequences of mutations in genes encoding proteins of the lectin pathway of complement activation, a central component of the innate immune system. Apart from impairment of immunity against microorganisms, it is known that hereditary deficiencies of this system predispose one to autoimmune conditions. Polymorphisms in complement genes are linked to, for example, atypical hemolytic uremia and age-dependent macular degeneration. The complement system comprises three convergent pathways of activation: the classical, the alternative, and the lectin pathway. The recently discovered lectin pathway is less studied, but polymorphisms in the plasma pattern-recognition molecule mannan-binding lectin (MBL) are known to impact its level, and polymorphisms in the MBL-associated serine protease-2 (MASP-2) result in defects of complement activation. Recent studies have described roles outside complement and immunity of another MBL-associated serine protease, MASP-3, in the etiology of 3MC syndrome, an autosomal-recessive disorder involving a spectrum of developmental features, including characteristic facial dysmorphism. Syndrome-causing mutations were identified in MASP1, encoding MASP-3 and two additional proteins, MASP-1 and MAp44. Furthermore, an association was discovered between 3MC syndrome and mutations in COLEC11, encoding CL-K1, another molecule of the lectin pathway. The findings were confirmed in zebrafish, indicating that MASP-3 and CL-K1 underlie an evolutionarily conserved pathway of embryonic development. Along with the discovery of a role of C1q in pruning synapses in mice, these recent advances point toward a broader role of complement in development. Here, we compare the functional immunologic consequences of "conventional" complement deficiencies with these newly described developmental roles.
[Mh] Termos MeSH primário: Ativação do Complemento/genética
Proteínas do Sistema Complemento/genética
Genes Letais
Mutação
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Animais
Colectinas/genética
Enzimas Ativadoras do Complemento/química
Enzimas Ativadoras do Complemento/genética
Seres Humanos
Camundongos
Polimorfismo Genético
Conformação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Collectins); 9007-36-7 (Complement System Proteins); EC 3.- (Complement Activating Enzymes)
[Em] Mês de entrada:1108
[Cu] Atualização por classe:170504
[Lr] Data última revisão:
170504
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110614
[St] Status:MEDLINE


  5 / 1273 MEDLINE  
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[PMID]:21426252
[Au] Autor:Varga L; Farkas H
[Ad] Endereço:3rd Department of Internal Medicine, Semmelweis University Budapest, H-1125 Kútvölgyi street 4, Budapest, Hungary. lvarga@kut.sote.hu
[Ti] Título:rhC1INH: a new drug for the treatment of attacks in hereditary angioedema caused by C1-inhibitor deficiency.
[So] Source:Expert Rev Clin Immunol;7(2):143-53, 2011 Mar.
[Is] ISSN:1744-8409
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Recombinant human C1 esterase inhibitor (rhC1INH) (Ruconest(®), Pharming) is a new drug developed for the relief of symptoms occurring in patients with angioedema due to C1-inhibitor deficiency. Pertinent results have already been published elsewhere; this article summarizes the progress made since then. Similar to the purified C1-inhibitor derived from human plasma, the therapeutic efficacy of rhC1INH results from its ability to block the actions of enzymes belonging to the overactivated bradykinin-forming pathway, at multiple locations. During clinical trials into the management of acute edema, a total of 190 subjects received recombinant C1-inhibitor by intravenous infusion on 714 occasions altogether. Dose-ranging efficacy studies established 50 U/kg as the recommended dose, and demonstrated the effectiveness of this agent in all localizations of hereditary angioedema attacks. Studies into the safety of rhC1INH based on 300 administrations to healthy subjects or hereditary angioedema patients followed-up for 90 days have not detected the formation of autoantibodies against rhC1INH or IgE antibodies directed against rabbit proteins, even after repeated administration on multiple occasions. These findings met favorable appraisal by the EMA, which granted European marketing authorization for rhC1INH. Pharming is expected to file a biological licence with the US FDA by the end of 2010 to obtain marketing approval in the USA. The launch of rhC1INH onto the pharmaceutical market may represent an important progress in the management of hereditary angioedema patients.
[Mh] Termos MeSH primário: Angioedemas Hereditários/tratamento farmacológico
Proteína Inibidora do Complemento C1/uso terapêutico
Proteínas Recombinantes/uso terapêutico
[Mh] Termos MeSH secundário: Angioedemas Hereditários/imunologia
Ensaios Clínicos como Assunto
Enzimas Ativadoras do Complemento/antagonistas & inibidores
Proteína Inibidora do Complemento C1/genética
Proteína Inibidora do Complemento C1/metabolismo
Proteína Inibidora do Complemento C1/farmacologia
Aprovação de Drogas
Europa (Continente)
Seres Humanos
Marketing
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Proteínas Recombinantes/farmacologia
Estados Unidos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Complement C1 Inhibitor Protein); 0 (Recombinant Proteins); EC 3.- (Complement Activating Enzymes)
[Em] Mês de entrada:1107
[Cu] Atualização por classe:110323
[Lr] Data última revisão:
110323
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110324
[St] Status:MEDLINE
[do] DOI:10.1586/eci.11.5


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[PMID]:21093502
[Au] Autor:Nakayama M; Hama C
[Ad] Endereço:Department of Molecular Biosciences, Faculty of Life Sciences, Kyoto Sangyo University, Kita-ku, Kyoto 603-8555, Japan.
[Ti] Título:Modulation of neurotransmitter receptors and synaptic differentiation by proteins containing complement-related domains.
[So] Source:Neurosci Res;69(2):87-92, 2011 Feb.
[Is] ISSN:1872-8111
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Neurotransmitter receptors play central roles in basic neurotransmission and synaptic plasticity. Recent studies have revealed that some transmembrane and extracellular proteins bind to neurotransmitter receptors, forming protein complexes that are required for proper synaptic localization or gating of core receptor molecules. Consequently, the components of these complexes contribute to long-term potentiation, a process that is critical for learning and memory. Here, we review factors that regulate neurotransmitter receptors, with a focus on proteins containing CUB (complement C1r/C1s, Uegf, Bmp1) or CCP (complement control protein) domains, which are frequently found in complement system proteins. Proteins that contain these domains are structurally distinct from TARPs (transmembrane AMPA receptor regulatory proteins), and may constitute new protein families that modulate either the localization or function of neurotransmitter receptors. In addition, other CCP domain-containing proteins participate in dendritic patterning and/or synaptic differentiation, although current evidence has not identified any direct activities on neurotransmitter receptors. Some of these proteins are involved in pathologic conditions such as epileptic seizure and mental retardation. Together, these lines of information have shown that CUB and CCP domain-containing proteins contribute to a wide variety of neuronal events that ultimately establish neural circuits.
[Mh] Termos MeSH primário: Diferenciação Celular
Plasticidade Neuronal/fisiologia
Receptores de Neurotransmissores/metabolismo
Sinapses/fisiologia
Transmissão Sináptica/fisiologia
[Mh] Termos MeSH secundário: Animais
Enzimas Ativadoras do Complemento/química
Enzimas Ativadoras do Complemento/metabolismo
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Receptors, Neurotransmitter); EC 3.- (Complement Activating Enzymes)
[Em] Mês de entrada:1104
[Cu] Atualização por classe:101224
[Lr] Data última revisão:
101224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:101125
[St] Status:MEDLINE
[do] DOI:10.1016/j.neures.2010.11.006


  7 / 1273 MEDLINE  
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[PMID]:20694009
[Au] Autor:Cardone J; Le Friec G; Vantourout P; Roberts A; Fuchs A; Jackson I; Suddason T; Lord G; Atkinson JP; Cope A; Hayday A; Kemper C
[Ad] Endereço:Division of Immunology, Infection and Inflammatory Diseases, King's College London, Medical Research Council Centre for Transplantation, Guy's Hospital, London, UK.
[Ti] Título:Complement regulator CD46 temporally regulates cytokine production by conventional and unconventional T cells.
[So] Source:Nat Immunol;11(9):862-71, 2010 Sep.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this study we demonstrate a new form of immunoregulation: engagement on CD4(+) T cells of the complement regulator CD46 promoted the effector potential of T helper type 1 cells (T(H)1 cells), but as interleukin 2 (IL-2) accumulated, it switched cells toward a regulatory phenotype, attenuating IL-2 production via the transcriptional regulator ICER/CREM and upregulating IL-10 after interaction of the CD46 tail with the serine-threonine kinase SPAK. Activated CD4(+) T cells produced CD46 ligands, and blocking CD46 inhibited IL-10 production. Furthermore, CD4(+) T cells in rheumatoid arthritis failed to switch, consequently producing excessive interferon-gamma (IFN-gamma). Finally, gammadelta T cells, which rarely produce IL-10, expressed an alternative CD46 isoform and were unable to switch. Nonetheless, coengagement of T cell antigen receptor (TCR) gammadelta and CD46 suppressed effector cytokine production, establishing that CD46 uses distinct mechanisms to regulate different T cell subsets during an immune response.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Citocinas/imunologia
Regulação da Expressão Gênica
Proteína Cofatora de Membrana/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/farmacologia
Linfócitos T CD4-Positivos/efeitos dos fármacos
Células CHO
Células Cultivadas
Enzimas Ativadoras do Complemento/imunologia
Cricetinae
Cricetulus
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Interleucina-10/imunologia
Interleucina-2/imunologia
Células Jurkat
Linfócitos T Auxiliares-Indutores/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (CD46 protein, human); 0 (Cytokines); 0 (Interleukin-2); 0 (Membrane Cofactor Protein); 130068-27-8 (Interleukin-10); EC 3.- (Complement Activating Enzymes)
[Em] Mês de entrada:1009
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100810
[St] Status:MEDLINE
[do] DOI:10.1038/ni.1917


  8 / 1273 MEDLINE  
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[PMID]:20300530
[Au] Autor:Cestari I; Ramirez MI
[Ad] Endereço:Laboratório de Biologia Molecular de Parasitas e Vetores, Instituto Oswaldo Cruz - Fiocruz, Rio de Janeiro, Brazil.
[Ti] Título:Inefficient complement system clearance of Trypanosoma cruzi metacyclic trypomastigotes enables resistant strains to invade eukaryotic cells.
[So] Source:PLoS One;5(3):e9721, 2010 Mar 16.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The complement system is the main arm of the vertebrate innate immune system against pathogen infection. For the protozoan Trypanosoma cruzi, the causative agent of Chagas disease, subverting the complement system and invading the host cells is crucial to succeed in infection. However, little attention has focused on whether the complement system can effectively control T. cruzi infection. To address this question, we decided to analyse: 1) which complement pathways are activated by T. cruzi using strains isolated from different hosts, 2) the capacity of these strains to resist the complement-mediated killing at nearly physiological conditions, and 3) whether the complement system could limit or control T. cruzi invasion of eukaryotic cells. The complement activating molecules C1q, C3, mannan-binding lectin and ficolins bound to all strains analysed; however, C3b and C4b deposition assays revealed that T. cruzi activates mainly the lectin and alternative complement pathways in non-immune human serum. Strikingly, we detected that metacyclic trypomastigotes of some T. cruzi strains were highly susceptible to complement-mediated killing in non-immune serum, while other strains were resistant. Furthermore, the rate of parasite invasion in eukaryotic cells was decreased by non-immune serum. Altogether, these results establish that the complement system recognizes T. cruzi metacyclic trypomastigotes, resulting in killing of susceptible strains. The complement system, therefore, acts as a physiological barrier which resistant strains have to evade for successful host infection.
[Mh] Termos MeSH primário: Trypanosoma cruzi/metabolismo
Glicoproteínas Variantes de Superfície de Trypanosoma/metabolismo
[Mh] Termos MeSH secundário: Animais
Cercopithecus aethiops
Enzimas Ativadoras do Complemento/metabolismo
Complemento C1q/metabolismo
Complemento C3/metabolismo
Complemento C3b/metabolismo
Complemento C4b/metabolismo
Ensaio de Imunoadsorção Enzimática/métodos
Cinética
Lectinas/química
Fígado/patologia
Modelos Biológicos
Células Vero
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Complement C3); 0 (Lectins); 0 (Variant Surface Glycoproteins, Trypanosoma); 0 (ficolin); 138820-03-8 (trypomastigote specific surface antigen); 80295-33-6 (Complement C1q); 80295-43-8 (Complement C3b); 80295-50-7 (Complement C4b); EC 3.- (Complement Activating Enzymes)
[Em] Mês de entrada:1101
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100320
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0009721


  9 / 1273 MEDLINE  
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[PMID]:20074261
[Au] Autor:Lynch AM; Murphy JR; Gibbs RS; Levine RJ; Giclas PC; Salmon JE; Holers VM
[Ad] Endereço:Department of Obstetrics and Gynecology, University of Colorado Denver School of Medicine, 12631 East 17th Avenue, Aurora, CO 80045, USA. anne.lynch@ucdenver.edu
[Ti] Título:The interrelationship of complement-activation fragments and angiogenesis-related factors in early pregnancy and their association with pre-eclampsia.
[So] Source:BJOG;117(4):456-62, 2010 Mar.
[Is] ISSN:1471-0528
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To determine the interrelationships during early pregnancy of complement-activation fragments Bb, C3a and sC5b-9, and angiogenesis-related factors placental growth factor (PiGF), soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng), and their associations with pre-eclampsia. DESIGN: Prospective cohort study. SETTING: Denver complement study (June 2005-June 2008). POPULATION: A total of 668 pregnant women with singleton gestations, recruited between 10 and 15 weeks of gestation. METHODS: Using univariable and multivariable logistic regression analysis, concentrations of complement-activation fragments and angiogenesis-related factors were compared between 10 and 15 weeks of gestation in women who subsequently did or did not develop pre-eclampsia. Interrelationships between these variables were tested using the non-parametric Spearman rank correlation coefficient. MAIN OUTCOME MEASURE: Pre-eclampsia. The association of complement-activation fragments and angiogenesis-related factors with obesity was also examined. RESULTS: The mean (+/-SD) levels of complement Bb in early pregnancy among women who did and did not develop pre-eclampsia were 0.84 (+/-0.26) microg/ml and 0.69 (+/-0.2) microg/ml, respectively (P = 0.001). Concentrations of PiGF were significantly (P = 0.01) lower (31 +/- 12 pg/ml) in early pregnancy in the pre-eclamptic group of women, as compared with the normotensive group (39 +/- 32 pg/ml). The adjusted odds ratio (AOR) of Bb and PiGF were 2.1 (CI = 1.4-3.1, P < 0.0003) and 0.2 (CI = 0.07-0.7, P = 0.01), respectively. There was no significant difference in the levels of C3a, sC5b-9, sFlt-1 and sEng in early pregnancy among women who developed pre-eclampsia, compared with women who remained normotensive during pregnancy. Higher levels of Bb (P = 0.0001) and C3a (P = 0.03), and lower levels of sFlt-1 (P = 0.0002) and sEng (P = 0.0001) were found among women with obesity, compared with non-obese controls. No meaningful relationships were found between the complement-activation fragments and the angiogenesis-related factors. CONCLUSIONS: In this cohort during early pregnancy, increased concentrations of complement-activation factor Bb and lower concentrations of PiGF were associated with the development of pre-eclampsia later in pregnancy.
[Mh] Termos MeSH primário: Antígenos CD/metabolismo
Enzimas Ativadoras do Complemento/metabolismo
Proteínas de Membrana/metabolismo
Obesidade/complicações
Pré-Eclâmpsia/etiologia
Receptores de Superfície Celular/metabolismo
Receptor 1 de Fatores de Crescimento do Endotélio Vascular/metabolismo
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/metabolismo
Endoglina
Feminino
Seres Humanos
Obesidade/metabolismo
Pré-Eclâmpsia/diagnóstico
Gravidez
Estudos Prospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, N.I.H., INTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Biomarkers); 0 (ENG protein, human); 0 (Endoglin); 0 (Membrane Proteins); 0 (PIGF protein, human); 0 (Receptors, Cell Surface); EC 2.7.10.1 (FLT1 protein, human); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-1); EC 3.- (Complement Activating Enzymes)
[Em] Mês de entrada:1006
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:100116
[St] Status:MEDLINE
[do] DOI:10.1111/j.1471-0528.2009.02473.x


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[PMID]:19667083
[Au] Autor:Liszewski MK; Leung MK; Hauhart R; Fang CJ; Bertram P; Atkinson JP
[Ad] Endereço:Department of Medicine, Division of Rheumatology, Washington University School of Medicine, St. Louis, MO 63110, USA.
[Ti] Título:Smallpox inhibitor of complement enzymes (SPICE): dissecting functional sites and abrogating activity.
[So] Source:J Immunol;183(5):3150-9, 2009 Sep 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although smallpox was eradicated as a global illness more than 30 years ago, variola virus and other related pathogenic poxviruses, such as monkeypox, remain potential bioterrorist weapons or could re-emerge as natural infections. Poxviruses express virulence factors that down-modulate the host's immune system. We previously compared functional profiles of the poxviral complement inhibitors of smallpox, vaccinia, and monkeypox known as SPICE, VCP (or VICE), and MOPICE, respectively. SPICE was the most potent regulator of human complement and attached to cells via glycosaminoglycans. The major goals of the present study were to further characterize the complement regulatory and heparin binding sites of SPICE and to evaluate a mAb that abrogates its function. Using substitution mutagenesis, we established that (1) elimination of the three heparin binding sites severely decreases but does not eliminate glycosaminoglycan binding, (2) there is a hierarchy of activity for heparin binding among the three sites, and (3) complement regulatory sites overlap with each of the three heparin binding motifs. By creating chimeras with interchanges of SPICE and VCP residues, a combination of two SPICE amino acids (H77 plus K120) enhances VCP activity approximately 200-fold. Also, SPICE residue L131 is critical for both complement regulatory function and accounts for the electrophoretic differences between SPICE and VCP. An evolutionary history for these structure-function adaptations of SPICE is proposed. Finally, we identified and characterized a mAb that inhibits the complement regulatory activity of SPICE, MOPICE, and VCP and thus could be used as a therapeutic agent.
[Mh] Termos MeSH primário: Enzimas Ativadoras do Complemento/antagonistas & inibidores
Enzimas Ativadoras do Complemento/metabolismo
Vírus da Varíola/imunologia
Proteínas da Matriz Viral/antagonistas & inibidores
Proteínas da Matriz Viral/fisiologia
[Mh] Termos MeSH secundário: Motivos de Aminoácidos/genética
Motivos de Aminoácidos/imunologia
Sequência de Aminoácidos
Animais
Anticorpos Monoclonais/metabolismo
Sítios de Ligação/genética
Sítios de Ligação/imunologia
Sítios de Ligação de Anticorpos
Células CHO
Enzimas Ativadoras do Complemento/genética
Complemento C3b/metabolismo
Cricetinae
Cricetulus
Glicosaminoglicanos/antagonistas & inibidores
Glicosaminoglicanos/metabolismo
Heparina/metabolismo
Seres Humanos
Hibridomas
Camundongos
Dados de Sequência Molecular
Mutação Puntual
Vírus da Varíola/genética
Vírus da Varíola/patogenicidade
Proteínas da Matriz Viral/genética
Proteínas da Matriz Viral/metabolismo
Fatores de Virulência/antagonistas & inibidores
Fatores de Virulência/genética
Fatores de Virulência/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Glycosaminoglycans); 0 (SPICE protein, variola virus); 0 (Viral Matrix Proteins); 0 (Virulence Factors); 80295-43-8 (Complement C3b); 9005-49-6 (Heparin); EC 3.- (Complement Activating Enzymes)
[Em] Mês de entrada:0909
[Cu] Atualização por classe:161122
[Lr] Data última revisão:
161122
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:090812
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.0901366



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