Base de dados : MEDLINE
Pesquisa : D12.776.395.550.294 [Categoria DeCS]
Referências encontradas : 324 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 33 ir para página                         

  1 / 324 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28863469
[Au] Autor:Tuikue Ndam N; Moussiliou A; Lavstsen T; Kamaliddin C; Jensen ATR; Mama A; Tahar R; Wang CW; Jespersen JS; Alao JM; Gamain B; Theander TG; Deloron P
[Ad] Endereço:UMR 216, Mère et enfant face aux infections tropicales, Institut de Recherche pour le développement, COMUE Sorbonne Paris Cité, Faculté de pharmacie, Laboratoire d'Excellence GR-Ex, DHU Risques et Grossesse, France.
[Ti] Título:Parasites Causing Cerebral Falciparum Malaria Bind Multiple Endothelial Receptors and Express EPCR and ICAM-1-Binding PfEMP1.
[So] Source:J Infect Dis;215(12):1918-1925, 2017 Jun 15.
[Is] ISSN:1537-6613
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) mediates the binding and accumulation of infected erythrocytes (IE) to blood vessels and tissues. Specific interactions have been described between PfEMP1 and human endothelial proteins CD36, intercellular adhesion molecule-1 (ICAM-1), and endothelial protein C receptor (EPCR); however, cytoadhesion patterns typical for pediatric malaria syndromes and the associated PfEMP1 members are still undefined. Methods: In a cohort of 94 hospitalized children with malaria, we characterized the binding properties of IE collected on admission, and var gene transcription using quantitative polymerase chain reaction. Results: IE from patients with cerebral malaria were more likely to bind EPCR and ICAM-1 than IE from children with uncomplicated malaria (P = .007). The level of transcripts encoding CIDRα1.4 and CIDRα1.5 domain subclasses was higher in patients with severe disease (P < .05). IE populations exhibiting binding to all 3 receptors had higher levels of transcripts encoding PfEMP1 with CIDRα1.4 and Duffy binding-like (DBL)-ß3 domains than parasites, which only bound CD36. Conclusions: These results underpin the significance of EPCR binding in pediatric malaria patients that require hospital admission, and support the notion that complementary receptor interactions of EPCR binding PfEMP1with ICAM-1 amplifies development of severe malaria symptoms.
[Mh] Termos MeSH primário: Antígenos CD/metabolismo
Molécula 1 de Adesão Intercelular/metabolismo
Malária Cerebral/parasitologia
Malária Falciparum/parasitologia
Plasmodium falciparum/metabolismo
Proteínas de Protozoários/metabolismo
Receptores de Superfície Celular/metabolismo
[Mh] Termos MeSH secundário: Adesão Celular
Pré-Escolar
Células Endoteliais/metabolismo
Receptor de Proteína C Endotelial
Seres Humanos
Lactente
Ligação Proteica
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Endothelial Protein C Receptor); 0 (PROCR protein, human); 0 (Protozoan Proteins); 0 (Receptors, Cell Surface); 0 (erythrocyte membrane protein 1, Plasmodium falciparum); 126547-89-5 (Intercellular Adhesion Molecule-1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170903
[St] Status:MEDLINE
[do] DOI:10.1093/infdis/jix230


  2 / 324 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28732053
[Au] Autor:Maknitikul S; Luplertlop N; Grau GER; Ampawong S
[Ad] Endereço:Department of Tropical Pathology, Faculty of Tropical Medicine, Mahidol University, Ratchathewi, Bangkok, Thailand.
[Ti] Título:Dysregulation of pulmonary endothelial protein C receptor and thrombomodulin in severe falciparum malaria-associated ARDS relevant to hemozoin.
[So] Source:PLoS One;12(7):e0181674, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To investigate the role of the protein C system, endothelial protein C receptor (EPCR) and thrombomodulin (TM) in the pathogenesis of malaria-associated acute respiratory distress syndrome (ARDS) in relation to hemozoin and proinflammatory cytokines-induced type II pneumocyte injury and -aggravated pulmonary resolution. A total of 29 left-over lung specimens that were obtained from patients who died from severe falciparum malaria were examined. Histopathological, immunohistochemical and electron microscopic analyses revealed that ARDS coexisted with pulmonary edema and systemic bleeding; the severity was dependent on the level of hemozoin deposition in the lung and internal alveolar hemorrhaging. The loss of EPCR and TM was primarily identified in ARDS patients and was related to the level of hemozoin, parasitized red blood cell (PRBC) and white blood cell accumulation in the lung. Moreover, an in vitro analysis demonstrated that interleukin-13 and -31 and hemozoin induced pneumocytic cell injury and apoptosis, as assessed by EB/AO staining, electron microscopy and the up-regulation of CARD-9 mRNA (caspase recruitment domain-9 messenger-ribonucleic acid). The dysregulation of EPCR and TM in the lung, especially in those with increased levels of hemozoin, may play an important role in the pathogenesis of malaria-associated ARDS through an apoptotic pathway.
[Mh] Termos MeSH primário: Antígenos CD/metabolismo
Hemeproteínas/uso terapêutico
Pulmão/metabolismo
Malária Falciparum/tratamento farmacológico
Receptores de Superfície Celular/metabolismo
Síndrome do Desconforto Respiratório do Adulto/metabolismo
Síndrome do Desconforto Respiratório do Adulto/parasitologia
Trombomodulina/metabolismo
[Mh] Termos MeSH secundário: Células A549
Adolescente
Adulto
Criança
Pré-Escolar
Citocinas/metabolismo
Receptor de Proteína C Endotelial
Feminino
Seres Humanos
Interleucina-13/metabolismo
Pulmão/parasitologia
Masculino
Meia-Idade
Proteína C/metabolismo
Edema Pulmonar/metabolismo
Edema Pulmonar/parasitologia
Regulação para Cima/efeitos dos fármacos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Cytokines); 0 (Endothelial Protein C Receptor); 0 (Hemeproteins); 0 (Interleukin-13); 0 (PROCR protein, human); 0 (Protein C); 0 (Receptors, Cell Surface); 0 (Thrombomodulin); 39404-00-7 (hemozoin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181674


  3 / 324 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28538400
[Au] Autor:Meng X; Fei D; Liu M; Yang S; Song N; Jiang L; Kang K; Nan C; Luo Y; Pan S; Zhao M
[Ad] Endereço:aDepartment of ICU bDepartment of Endocrinology cThe Key Hepatosplenic Surgery Laboratory, Department of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
[Ti] Título:Carbon monoxide-releasing molecule-2 suppresses thrombomodulin and endothelial protein C receptor expression of human umbilical vein endothelial cells induced by lipopolysaccharide in vitro.
[So] Source:Medicine (Baltimore);96(21):e6978, 2017 May.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The aim of this study was to observe the counter-effect of carbon monoxide-releasing molecule-2 (CORM-2) on lipopolysaccharide (LPS)-suppressed thrombomodulin (TM) and endothelial protein C receptor (EPCR) expressions from human umbilical vein endothelial cell (HUVEC), and to reveal its mechanisms. METHODS: HUVECs were divided into 5 treatment groups, wherein reagents were added simultaneously. TM and EPCR proteins of the cells and the culture medium levels of soluble TM, soluble EPCR, and matrix metalloproteinase-2 (MMP-2) were detected after administration, whereas mRNA levels of TM and EPCR, as well as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activity among groups, were also evaluated. RESULTS: No significant difference was observed in any indicator between CORM-2 and sham groups. Addition of LPS produced drastic increase in MMP-2 expression, NF-κB activity, shedding of TM and EPCR (into the culture medium), as well as remarkable decrease in both mRNA and protein expressions of TM and EPCR, and cell viability. LPS + CORM-2 treatment significantly reduced the increase in MMP-2, NF-κB activity, and TM/EPCR shedding, whereas maintained both mRNA and protein levels of TM and EPCR, and preserved cell viability. CONCLUSIONS: CORM-2 protects HUVEC from LPS-induced injury, by way of suppressing NF-κB activity, which downregulates TM and EPCR mRNAs. It also decreases MMP-2 expression and prevents the shedding of TM and EPCR from the surface of endothelial cells, so as to preserve their protective effect.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Antígenos CD/metabolismo
Fármacos Cardiovasculares/farmacologia
Compostos Organometálicos/farmacologia
Receptores de Superfície Celular/metabolismo
Trombomodulina/metabolismo
[Mh] Termos MeSH secundário: Técnicas de Cultura de Células
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/fisiologia
Avaliação Pré-Clínica de Medicamentos
Receptor de Proteína C Endotelial
Escherichia coli
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Lipopolissacarídeos
Metaloproteinase 2 da Matriz/metabolismo
NF-kappa B/metabolismo
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antigens, CD); 0 (Cardiovascular Agents); 0 (Endothelial Protein C Receptor); 0 (Lipopolysaccharides); 0 (NF-kappa B); 0 (Organometallic Compounds); 0 (PROCR protein, human); 0 (RNA, Messenger); 0 (Receptors, Cell Surface); 0 (THBD protein, human); 0 (Thrombomodulin); 0 (tricarbonyldichlororuthenium (II) dimer); EC 3.4.24.24 (MMP2 protein, human); EC 3.4.24.24 (Matrix Metalloproteinase 2)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170525
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000006978


  4 / 324 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28415941
[Au] Autor:Liang Y; Huang X; Jiang Y; Qin Y; Peng D; Huang Y; Li J; Sooranna SR; Pinhu L
[Ad] Endereço:1 Affiliated Hospital of Youjiang Medical University, Baise, Guangxi, PR China.
[Ti] Título:Endothelial protein C receptor polymorphisms and risk of sepsis in a Chinese population.
[So] Source:J Int Med Res;45(2):504-513, 2017 Apr.
[Is] ISSN:1473-2300
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Objective To examine the potential relationship of EPCR polymorphisms and the risk of sepsis in a Chinese population. Methods Snapshot SNP genotyping assays and DNA sequencing methods were used to detect polymorphisms of the EPCR gene, rs2069948C/T (2532C/T) and rs867186A/G (6936A/G), in 64 patients with sepsis and in 113 controls. Soluble EPCR (sEPCR) was measured by ELISA. Results There were significant differences in the allele and genotype frequencies of EPCR gene rs2069948C/T and allele frequencies of rs867186A/G between male and female patients and controls. Females carrying rs2069948 C/T genotype or T allele and males carrying rs867186 A allele were associated with a significantly increased risk of sepsis. Plasma sEPCR levels of sepsis patients were higher than controls and showed no correlation with EPCR gene polymorphisms. Conclusions EPCR polymorphisms may be associated with increased risk of sepsis, but this has no effect on the release of sEPCR in patients with sepsis.
[Mh] Termos MeSH primário: Antígenos CD/genética
Predisposição Genética para Doença
Polimorfismo de Nucleotídeo Único
Receptores de Superfície Celular/genética
Sepse/diagnóstico
Sepse/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Alelos
Antígenos CD/sangue
Grupo com Ancestrais do Continente Asiático
Estudos de Casos e Controles
Receptor de Proteína C Endotelial
Feminino
Expressão Gênica
Frequência do Gene
Seres Humanos
Masculino
Meia-Idade
Receptores de Superfície Celular/sangue
Risco
Sepse/etnologia
Sepse/patologia
Análise de Sequência de DNA
Fatores Sexuais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Endothelial Protein C Receptor); 0 (PROCR protein, human); 0 (Receptors, Cell Surface)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170419
[St] Status:MEDLINE
[do] DOI:10.1177/0300060516686496


  5 / 324 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28408624
[Au] Autor:Healy LD; Puy C; Fernández JA; Mitrugno A; Keshari RS; Taku NA; Chu TT; Xu X; Gruber A; Lupu F; Griffin JH; McCarty OJT
[Ad] Endereço:From the Departments of Cell, Developmental & Cancer Biology and healyl@ohsu.edu.
[Ti] Título:Activated protein C inhibits neutrophil extracellular trap formation and activation .
[So] Source:J Biol Chem;292(21):8616-8629, 2017 May 26.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Activated protein C (APC) is a multifunctional serine protease with anticoagulant, cytoprotective, and anti-inflammatory activities. In addition to the cytoprotective effects of APC on endothelial cells, podocytes, and neurons, APC cleaves and detoxifies extracellular histones, a major component of neutrophil extracellular traps (NETs). NETs promote pathogen clearance but also can lead to thrombosis; the pathways that negatively regulate NETosis are largely unknown. Thus, we studied whether APC is capable of directly inhibiting NETosis via receptor-mediated cell signaling mechanisms. Here, by quantifying extracellular DNA or myeloperoxidase, we demonstrate that APC binds human leukocytes and prevents activated platelet supernatant or phorbol 12-myristate 13-acetate (PMA) from inducing NETosis. Of note, APC proteolytic activity was required for inhibiting NETosis. Moreover, antibodies against the neutrophil receptors endothelial protein C receptor (EPCR), protease-activated receptor 3 (PAR3), and macrophage-1 antigen (Mac-1) blocked APC inhibition of NETosis. Select mutations in the Gla and protease domains of recombinant APC caused a loss of NETosis. Interestingly, pretreatment of neutrophils with APC prior to induction of NETosis inhibited platelet adhesion to NETs. Lastly, in a nonhuman primate model of -induced sepsis, pretreatment of animals with APC abrogated release of myeloperoxidase from neutrophils, a marker of neutrophil activation. These findings suggest that the anti-inflammatory function of APC at therapeutic concentrations may include the inhibition of NETosis in an EPCR-, PAR3-, and Mac-1-dependent manner, providing additional mechanistic insight into the diverse functions of neutrophils and APC in disease states including sepsis.
[Mh] Termos MeSH primário: Armadilhas Extracelulares/imunologia
Ativação de Neutrófilo/imunologia
Neutrófilos/imunologia
Proteína C/imunologia
[Mh] Termos MeSH secundário: Animais
Antígenos CD/imunologia
Antígenos CD/metabolismo
Modelos Animais de Doenças
Receptor de Proteína C Endotelial
Escherichia coli
Infecções por Escherichia coli/sangue
Infecções por Escherichia coli/imunologia
Armadilhas Extracelulares/metabolismo
Feminino
Seres Humanos
Antígeno de Macrófago 1/imunologia
Antígeno de Macrófago 1/metabolismo
Masculino
Ativação de Neutrófilo/efeitos dos fármacos
Neutrófilos/metabolismo
Papio anubis
Proteína C/metabolismo
Receptores de Superfície Celular/imunologia
Receptores de Superfície Celular/metabolismo
Sepse/sangue
Sepse/imunologia
Acetato de Tetradecanoilforbol/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Endothelial Protein C Receptor); 0 (Macrophage-1 Antigen); 0 (PROCR protein, human); 0 (Protein C); 0 (Receptors, Cell Surface); NI40JAQ945 (Tetradecanoylphorbol Acetate)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170415
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.768309


  6 / 324 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28408459
[Au] Autor:Fares I; Chagraoui J; Lehnertz B; MacRae T; Mayotte N; Tomellini E; Aubert L; Roux PP; Sauvageau G
[Ad] Endereço:Molecular Genetics of Stem Cells Laboratory.
[Ti] Título:EPCR expression marks UM171-expanded CD34 cord blood stem cells.
[So] Source:Blood;129(25):3344-3351, 2017 Jun 22.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A small subset of human cord blood CD34 cells express endothelial protein C receptor (EPCR/CD201/PROCR) when exposed to the hematopoietic stem cell (HSC) self-renewal agonist UM171. In this article, we show that EPCR-positive UM171-treated cells, as opposed to EPCR-negative cells, exhibit robust multilineage repopulation and serial reconstitution ability in immunocompromised mice. In contrast to other stem cell markers, such as CD38, EPCR expression is maintained when cells are introduced in culture, irrespective of UM171 treatment. Although engineered overexpression of EPCR fails to reproduce the effects of UM171 on HSC activity, its expression is required for the repopulating activity of human HSCs. Altogether, our results indicate that EPCR is a reliable and cell culture-compatible marker of UM171-expanded human cord blood HSCs.
[Mh] Termos MeSH primário: Antígenos CD34/análise
Antígenos CD/análise
Sangue Fetal/citologia
Células-Tronco Hematopoéticas/efeitos dos fármacos
Indóis/farmacologia
Pirimidinas/farmacologia
Receptores de Superfície Celular/análise
[Mh] Termos MeSH secundário: Animais
Técnicas de Cultura de Células
Proliferação Celular/efeitos dos fármacos
Receptor de Proteína C Endotelial
Feminino
Transplante de Células-Tronco Hematopoéticas
Células-Tronco Hematopoéticas/citologia
Seres Humanos
Camundongos Endogâmicos NOD
Camundongos SCID
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, CD34); 0 (Endothelial Protein C Receptor); 0 (Indoles); 0 (PROCR protein, human); 0 (Pyrimidines); 0 (Receptors, Cell Surface); 0 (UM171 compound)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170415
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2016-11-750729


  7 / 324 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28367652
[Au] Autor:Ma Y; Zhao Y; Zhang R; Liang X; Yin Z; Geng Y; Shu G; Song X; Zou Y; Li L; Yin L; Yue G; Li Y; Ye G; He C
[Ad] Endereço:a Natural Medicine Research Center, College of Veterinary Medicine , Sichuan Agricultural University , Chengdu , PR China.
[Ti] Título:Astragaloside IV inhibits PMA-induced EPCR shedding through MAPKs and PKC pathway.
[So] Source:Immunopharmacol Immunotoxicol;39(3):148-156, 2017 Jun.
[Is] ISSN:1532-2513
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Astragaloside IV (AS-IV), a main active substance isolated from Astragalus membranaceus Bunge, has been shown to have multiple pharmacological effects. Endothelial cell protein C receptor (EPCR) is a marker of inflammation, and is also a major member of protein C (PC) anti-coagulation system. EPCR can be cut off from the cell surface by tumor necrosis factor-α converting enzyme (TACE), which is controlled through mitogen-activated protein kinase (MAPK) and protein kinase C (PKC) pathways. To develop novel therapeutic drug for EPCR shedding, the effect of AS-IV was studied in phorbol-12-myristate 13-acetate (PMA)-induced human umbilical vein endothelial cells (HUVECs) and the potential molecular mechanism of AS-IV action was investigated. The results showed that AS-IV could significantly inhibit PMA-induced EPCR shedding. In further study, AS-IV suppressed the expression and activity of TACE. In addition, AS-IV could decrease the phosphorylation of MAPK such as janus kinase (JNK) and p38, and inhibit activation of PKC through the prevention of non-phosphorylation and phosphorylation of specific PKC isoforms in PMA-stimulated HUVECs. These findings indicate that AS-IV may be used as a natural medicine to treat EPCR-related systemic inflammation and cardiovascular diseases by targeting MAPK and PKC pathway.
[Mh] Termos MeSH primário: Antígenos CD/imunologia
MAP Quinases Reguladas por Sinal Extracelular/imunologia
Células Endoteliais da Veia Umbilical Humana/imunologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Proteína Quinase C/imunologia
Receptores de Superfície Celular/imunologia
Saponinas/farmacologia
Acetato de Tetradecanoilforbol/farmacologia
Triterpenos/farmacologia
[Mh] Termos MeSH secundário: Receptor de Proteína C Endotelial
Células Endoteliais da Veia Umbilical Humana/citologia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Endothelial Protein C Receptor); 0 (PROCR protein, human); 0 (Receptors, Cell Surface); 0 (Saponins); 0 (Triterpenes); 3A592W8XKE (astragaloside A); EC 2.7.11.13 (Protein Kinase C); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); NI40JAQ945 (Tetradecanoylphorbol Acetate)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE
[do] DOI:10.1080/08923973.2017.1306868


  8 / 324 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28353616
[Au] Autor:Jiang J; Liu K; Zou J; Ma H; Yang H; Zhang X; Jiao Y
[Ad] Endereço:aDivision of Vascular Surgery, Department of General Surgery bDepartment of Nephrology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.
[Ti] Título:Associations between polymorphisms in coagulation-related genes and venous thromboembolism: A meta-analysis with trial sequential analysis.
[So] Source:Medicine (Baltimore);96(13):e6537, 2017 Mar.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Recently, several studies showed that the polymorphisms in the coagulation-related genes might be associated with venous thromboembolism (VTE); however, the results were still controversial. We performed a meta-analysis with trial sequential analysis to investigate the associations between the endothelial cell-activated protein C receptor (EPCR) rs9574, F11 rs2289252, F11 rs2036914, FGG rs2066865, FGG rs1049636, CYP4V2 rs13146272, SERPINC1 rs2227589, and GP6 rs1613662 polymorphisms with the risk of VTE. METHODS: We searched both the common English-language databases and the Chinese literature databases. Two authors selected studies according to inclusion and exclusion criteria. Crude odds ratios with 95% confidence intervals (CI) were calculated to estimate the strength of this association. Between-study heterogeneity was assessed with the chi-square-based Q test and the I statistic. RESULTS: Overall, a total of 20 studies were included. The meta-analysis revealed that the F11 rs2289252, F11 rs2036914, FGG rs2066865, and CYP4V2 rs13146272 polymorphisms were closely related to the development of VTE in the white race under the best genetic models after multiple testing adjustments. The EPCR rs9574, FGG rs1049636, SERPINC1 rs2227589, and GP6 rs1613662 polymorphisms might be potential candidates in the pathogenesis of VTE, but trial sequential analyses and sensitivity analyses indicated that the evidences were limited. Larger scale studies were demanded to avoid false-positive outcomes. CONCLUSIONS: Finally, our study demonstrated the important role of rs2289252, rs2036914, rs2066865, and rs13146272 polymorphisms in the development of VTE in the white race. Rs9574, rs1049636, rs2227589 and rs1613662 polymorphisms might be risk factors of VTE. However, more studies involving diverse races are needed to probe the ethnic difference and the underlying mechanisms of significant associations.
[Mh] Termos MeSH primário: Família 4 do Citocromo P450/genética
Fator XI/genética
Fibrinogênio/genética
Tromboembolia Venosa/genética
[Mh] Termos MeSH secundário: Antígenos CD/genética
Antitrombina III/genética
Receptor de Proteína C Endotelial
Seres Humanos
Glicoproteínas da Membrana de Plaquetas/genética
Receptores de Superfície Celular/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Endothelial Protein C Receptor); 0 (PROCR protein, human); 0 (Platelet Membrane Glycoproteins); 0 (Receptors, Cell Surface); 0 (SERPINC1 protein, human); 0 (platelet membrane glycoprotein VI); 9000-94-6 (Antithrombin III); 9001-32-5 (Fibrinogen); 9013-55-2 (Factor XI); EC 1.14.13.- (CYP4V2 protein, human); EC 1.14.14.1 (Cytochrome P450 Family 4)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170330
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000006537


  9 / 324 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28279348
[Au] Autor:Lennartz F; Adams Y; Bengtsson A; Olsen RW; Turner L; Ndam NT; Ecklu-Mensah G; Moussiliou A; Ofori MF; Gamain B; Lusingu JP; Petersen JE; Wang CW; Nunes-Silva S; Jespersen JS; Lau CK; Theander TG; Lavstsen T; Hviid L; Higgins MK; Jensen AT
[Ad] Endereço:Department of Biochemistry, University of Oxford, South Parks Road, OX1 3QU Oxford, UK.
[Ti] Título:Structure-Guided Identification of a Family of Dual Receptor-Binding PfEMP1 that Is Associated with Cerebral Malaria.
[So] Source:Cell Host Microbe;21(3):403-414, 2017 Mar 08.
[Is] ISSN:1934-6069
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cerebral malaria is a deadly outcome of infection by Plasmodium falciparum, occurring when parasite-infected erythrocytes accumulate in the brain. These erythrocytes display parasite proteins of the PfEMP1 family that bind various endothelial receptors. Despite the importance of cerebral malaria, a binding phenotype linked to its symptoms has not been identified. Here, we used structural biology to determine how a group of PfEMP1 proteins interacts with intercellular adhesion molecule 1 (ICAM-1), allowing us to predict binders from a specific sequence motif alone. Analysis of multiple Plasmodium falciparum genomes showed that ICAM-1-binding PfEMP1s also interact with endothelial protein C receptor (EPCR), allowing infected erythrocytes to synergistically bind both receptors. Expression of these PfEMP1s, predicted to bind both ICAM-1 and EPCR, is associated with increased risk of developing cerebral malaria. This study therefore reveals an important PfEMP1-binding phenotype that could be targeted as part of a strategy to prevent cerebral malaria.
[Mh] Termos MeSH primário: Adesão Celular
Malária Cerebral/parasitologia
Malária Falciparum/parasitologia
Plasmodium falciparum/patogenicidade
Proteínas de Protozoários/metabolismo
Fatores de Virulência/metabolismo
[Mh] Termos MeSH secundário: Antígenos CD/metabolismo
Biologia Computacional
Cristalografia por Raios X
Receptor de Proteína C Endotelial
Genoma de Protozoário
Molécula 1 de Adesão Intercelular/metabolismo
Plasmodium falciparum/fisiologia
Ligação Proteica
Proteínas de Protozoários/química
Proteínas de Protozoários/genética
Receptores de Superfície Celular/metabolismo
Espalhamento a Baixo Ângulo
Análise de Sequência de DNA
Ressonância de Plasmônio de Superfície
Fatores de Virulência/química
Fatores de Virulência/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Endothelial Protein C Receptor); 0 (PROCR protein, human); 0 (Protozoan Proteins); 0 (Receptors, Cell Surface); 0 (Virulence Factors); 0 (erythrocyte membrane protein 1, Plasmodium falciparum); 126547-89-5 (Intercellular Adhesion Molecule-1)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170311
[St] Status:MEDLINE


  10 / 324 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28219843
[Au] Autor:Pepler L; Wu C; Dwivedi DJ; Wu C; Kim PY; Liaw PC
[Ad] Endereço:Department of Medical Sciences at McMaster University, Hamilton, Ontario L8L 0A6, Canada; Thrombosis and Atherosclerosis Research Institute, Hamilton, Ontario L8L 0A6, Canada.
[Ti] Título:The impact of the endothelial protein C receptor on thrombin generation and clot lysis.
[So] Source:Thromb Res;152:30-37, 2017 Apr.
[Is] ISSN:1879-2472
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: When thrombin is bound to thrombomodulin (TM), it becomes a potent activator of protein C (PC) and thrombin-activable fibrinolysis inhibitor (TAFI). Activation of PC is enhanced when PC is bound to the endothelial protein C receptor (EPCR). Activated protein C (APC) inhibits thrombin generation while activated TAFI (TAFIa) attenuates fibrinolysis. To determine the impact of diminished EPCR function on thrombin generation and fibrinolysis we generated cells that expressed TM and a variant of EPCR (R96C) that does not bind PC. METHODS: To determine the impact of EPCR on the generation of APC and TAFIa and how this affects thrombin generation and fibrinolysis we performed thrombin generation and clot lysis assays in the presence of cells expressing wild-type TM and EPCR (WT cells) or wild-type TM and the R96C variant of EPCR (R96C cells). RESULTS: In the presence of R96C cells, thrombin generation in normal plasma is increased, as a result of impaired PC activation when compared to WT cells. In addition, clot lysis is delayed in normal plasma in the presence of R96C cells, despite no increase in TAFI activation. In PC deficient plasma, clot lysis is delayed in the presence of WT and R96C cells as a result of increased TAFI activation. CONCLUSIONS: We demonstrate that impaired EPCR function can be detected by thrombin generation and clot lysis assays on cells expressing TM and EPCR. We also demonstrated that deficiency in EPCR has procoagulant effects that lead to a delay in clot lysis.
[Mh] Termos MeSH primário: Antígenos CD/metabolismo
Fibrinólise
Receptores de Superfície Celular/metabolismo
Trombina/metabolismo
[Mh] Termos MeSH secundário: Coagulação Sanguínea
Carboxipeptidase B2/metabolismo
Linhagem Celular
Receptor de Proteína C Endotelial
Ativação Enzimática
Tempo de Lise do Coágulo de Fibrina
Células HEK293
Seres Humanos
Proteína C/metabolismo
Trombomodulina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Endothelial Protein C Receptor); 0 (PROCR protein, human); 0 (Protein C); 0 (Receptors, Cell Surface); 0 (Thrombomodulin); EC 3.4.17.20 (CPB2 protein, human); EC 3.4.17.20 (Carboxypeptidase B2); EC 3.4.21.5 (Thrombin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170222
[St] Status:MEDLINE



página 1 de 33 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde