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[PMID]:29399876
[Au] Autor:Martínez-García S; Rodríguez-Martínez S; Cancino-Diaz ME; Cancino-Diaz JC
[Ad] Endereço:Departamento de Microbiología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Ciudad de México, Mexico.
[Ti] Título:Extracellular proteases of Staphylococcus epidermidis: roles as virulence factors and their participation in biofilm.
[So] Source:APMIS;126(3):177-185, 2018 Mar.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Staphylococci produce a large number of extracellular proteases, some of which are considered as potential virulence factors. Staphylococcus epidermidis is a causative agent of nosocomial infections in medical devices by the formation of biofilms. It has been proposed that proteases contribute to the different stages of biofilm formation. S. epidermidis secretes a small number of extracellular proteases, such as serine protease Esp, cysteine protease EcpA, and metalloprotease SepA that have a relatively low substrate specificity. Recent findings indicate a significant contribution of extracellular proteases in biofilm formation through the proteolytic inactivation of adhesion molecules. The objective of this work is to provide an overview of the current knowledge of S. epidermidis' extracellular proteases during pathogenicity, especially in the different stages of biofilm formation.
[Mh] Termos MeSH primário: Proteínas de Bactérias/metabolismo
Biofilmes/crescimento & desenvolvimento
Cisteína Proteases/metabolismo
Metaloendopeptidases/metabolismo
Serina Proteases/metabolismo
Staphylococcus epidermidis/enzimologia
[Mh] Termos MeSH secundário: Moléculas de Adesão Celular/metabolismo
Infecção Hospitalar/microbiologia
Infecção Hospitalar/patologia
Seres Humanos
Infecções Estafilocócicas/microbiologia
Infecções Estafilocócicas/patologia
Staphylococcus epidermidis/metabolismo
Staphylococcus epidermidis/patogenicidade
Fatores de Virulência/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Cell Adhesion Molecules); 0 (Virulence Factors); EC 3.4.- (Cysteine Proteases); EC 3.4.- (Serine Proteases); EC 3.4.24.- (Metalloendopeptidases); EC 3.4.24.- (SepA protein, Staphylococcus epidermidis)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180206
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12805


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[PMID]:29381773
[Au] Autor:Moradi N; Fadaei R; Emamgholipour S; Kazemian E; Panahi G; Vahedi S; Saed L; Fallah S
[Ad] Endereço:Department of Clinical Biochemistry, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran.
[Ti] Título:Association of circulating CTRP9 with soluble adhesion molecules and inflammatory markers in patients with type 2 diabetes mellitus and coronary artery disease.
[So] Source:PLoS One;13(1):e0192159, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:C1q/TNF-related protein 9 (CTRP9) is a paralogue of adiponectin with known favorable effects on lipid and glucose metabolism. A potential role of CTRP9 for regulation of endothelium function has been suggested by previous studies. However, no studies have examined the relation between serum CTRP9 levels and adhesion molecules in patients with type 2 diabetes mellitus (T2DM) and coronary artery disease (CAD). The present study was conducted on 337 subjects who underwent coronary angiography and were categorized into four groups according to the presence of CAD and T2DM (control, CAD, T2DM and CAD+T2DM). Serum levels of CTRP9, adiponectin, sICAM-1, sVCAM-1, sE-Selectin, IL-6 and TNF-α were measured. It was found that the circulating CTRP9 levels were independently associated with increased risk of CAD and T2DM in addition to elevated levels of serum CTRP9 in CAD, T2DM and CAD+T2DM groups. A significant association of serum CTRP9 levels with adhesion molecules in CAD and T2DM patients as well as serum TNF-α levels in CAD individuals was noted. A significant relation between the circulating levels of CTRP9 and HOMA-IR in T2DM subjects was also observed. The results revealed increased circulating levels of CTRP9 in T2DM and CAD individuals which suggests a compensatory response to insulin resistance, inflammatory milieu and endothelial dysfunction; however, more studies are needed to confirm this.
[Mh] Termos MeSH primário: Adiponectina/sangue
Biomarcadores/sangue
Moléculas de Adesão Celular/sangue
Doença da Artéria Coronariana/sangue
Diabetes Mellitus Tipo 2/sangue
Glicoproteínas/sangue
Mediadores da Inflamação/sangue
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adiponectin); 0 (Biomarkers); 0 (C1QTNF9B protein, human); 0 (Cell Adhesion Molecules); 0 (Glycoproteins); 0 (Inflammation Mediators)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180131
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0192159


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[PMID]:28453729
[Au] Autor:Chen Z; Xie J; Hao H; Lin H; Wang L; Zhang Y; Chen L; Cao S; Huang X; Liao W; Bin J; Liao Y
[Ad] Endereço:State Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, 1838, Guangzhou Avenue North, Guangzhou 510515, China.
[Ti] Título:Ablation of periostin inhibits post-infarction myocardial regeneration in neonatal mice mediated by the phosphatidylinositol 3 kinase/glycogen synthase kinase 3ß/cyclin D1 signalling pathway.
[So] Source:Cardiovasc Res;113(6):620-632, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: To resolve the controversy as to whether periostin plays a role in myocardial regeneration after myocardial infarction (MI), we created a neonatal mouse model of MI to investigate the influence of periostin ablation on myocardial regeneration and clarify the underlying mechanisms. Methods and results: Neonatal periostin-knockout mice and their wildtype littermates were subjected to MI or sham surgery. In the wildtype mice after MI, fibrosis was detectable at 3 days and fibrotic tissue was completely replaced by regenerated myocardium at 21 days. In contrast, in the knockout mice, significant fibrosis in the infarcted area was present at even 3 weeks after MI. Levels of phosphorylated-histone 3 and aurora B in the myocardium, detected by immunofluorescence and western blotting, were significantly lower in knockout than in wildtype mice at 7 days after MI. Similarly, angiogenesis was decreased in the knockout mice after MI. Expression of both the endothelial marker CD-31 and α-smooth muscle actin was markedly lower in the knockout than in wildtype mice at 7 days after MI. The knockout MI group had elevated levels of glycogen synthase kinase (GSK) 3ß and decreased phosphatidylinositol 3-kinase (PI3K), phosphorylated serine/threonine protein kinase B (p-Akt), and cyclin D1, compared with the wildtype MI group. Similar effects were observed in experiments using cultured cardiomyocytes from neonatal wildtype or periostin knockout mice. Administration of SB216763, a GSK3ß inhibitor, to knockout neonatal mice decreased myocardial fibrosis and increased angiogenesis in the infarcted area after MI. Conclusion: Ablation of periostin suppresses post-infarction myocardial regeneration by inhibiting the PI3K/GSK3ß/cyclin D1 signalling pathway, indicating that periostin is essential for myocardial regeneration.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/deficiência
Ciclina D1/metabolismo
Infarto do Miocárdio/enzimologia
Miocárdio/enzimologia
Fosfatidilinositol 3-Quinase/metabolismo
Regeneração
Proteínas Repressoras/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Moléculas de Adesão Celular/genética
Células Cultivadas
Modelos Animais de Doenças
Fibrose
Camundongos Knockout
Infarto do Miocárdio/genética
Infarto do Miocárdio/patologia
Infarto do Miocárdio/fisiopatologia
Miocárdio/patologia
Neovascularização Fisiológica
Fosforilação
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas c-akt/metabolismo
Regeneração/efeitos dos fármacos
Proteínas Repressoras/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccnd1 protein, mouse); 0 (Cell Adhesion Molecules); 0 (GSKIP protein, mouse); 0 (Postn protein, mouse); 0 (Protein Kinase Inhibitors); 0 (Repressor Proteins); 136601-57-5 (Cyclin D1); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvx001


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[PMID]:29259037
[Au] Autor:Falch CM; Sundaram AYM; Øystese KA; Normann KR; Lekva T; Silamikelis I; Eieland AK; Andersen M; Bollerslev J; Olarescu NC
[Ad] Endereço:Section of Specialized EndocrinologyDepartment of Endocrinology cafal14@student.sdu.dk.
[Ti] Título:Gene expression profiling of fast- and slow-growing non-functioning gonadotroph pituitary adenomas.
[So] Source:Eur J Endocrinol;178(3):295-307, 2018 Mar.
[Is] ISSN:1479-683X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Reliable biomarkers associated with aggressiveness of non-functioning gonadotroph adenomas (GAs) are lacking. As the growth of tumor remnants is highly variable, molecular markers for growth potential prediction are necessary. We hypothesized that fast- and slow-growing GAs present different gene expression profiles and reliable biomarkers for tumor growth potential could be identified, focusing on the specific role of epithelial-mesenchymal transition (EMT). DESIGN AND METHODS: Eight GAs selected for RNA sequencing were equally divided into fast- and slow-growing group by the tumor volume doubling time (TVDT) median (27.75 months). Data were analyzed by tophat2, cufflinks and cummeRbund pipeline. 40 genes were selected for RT-qPCR validation in 20 GAs based on significance, fold-change and pathway analyses. The effect of silencing (metadherin) and (endomucin) on migration of human adenoma cells was evaluated. RESULTS: 350 genes were significantly differentially expressed (282 genes upregulated and 68 downregulated in the fast group, -adjusted <0.05). Among 40 selected genes, 11 showed associations with TVDT (-0.669< <-0.46, < 0.05). These were and six EMT-related genes ( and ). , but not , demonstrated involvement in cell migration and association with EMT markers. CONCLUSIONS: Fast- and slow-growing GAs present different gene expression profiles, and genes related to EMT have higher expression in fast-growing tumors. In addition to , identified as an important contributor to aggressiveness, the other genes might represent markers for tumor growth potential and possible targets for drug therapy.
[Mh] Termos MeSH primário: Adenoma/genética
Transição Epitelial-Mesenquimal/genética
Neoplasias Hipofisárias/genética
RNA Mensageiro/metabolismo
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética
Adenoma/metabolismo
Adulto
Idoso
Caderinas/genética
Moléculas de Adesão Celular/genética
Movimento Celular/genética
Subunidades Catalíticas da Proteína Quinase Dependente de AMP Cíclico/genética
Feminino
Hormônio Foliculoestimulante/metabolismo
Perfilação da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Inativação Gênica
Seres Humanos
Técnicas In Vitro
Peptídeos e Proteínas de Sinalização Intracelular/genética
Hormônio Luteinizante/metabolismo
Masculino
Glicoproteínas de Membrana/genética
Proteínas Associadas aos Microtúbulos/genética
Meia-Idade
Miosina Tipo I/genética
Proteínas do Tecido Nervoso/genética
Neoplasias Hipofisárias/metabolismo
Proteínas Proto-Oncogênicas/genética
Receptores de Superfície Celular/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Ribonucleases/genética
Sialoglicoproteínas/genética
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Cadherins); 0 (Cell Adhesion Molecules); 0 (EMCN protein, human); 0 (GPM6A protein, human); 0 (Intracellular Signaling Peptides and Proteins); 0 (MTDH protein, human); 0 (MYO1B protein, human); 0 (Membrane Glycoproteins); 0 (Microtubule-Associated Proteins); 0 (Nerve Tissue Proteins); 0 (PCDH18 protein, human); 0 (Proto-Oncogene Proteins); 0 (RNA, Messenger); 0 (Receptors, Cell Surface); 0 (SKIL protein, human); 0 (SPAG9 protein, human); 0 (Sialoglycoproteins); 0 (UNC5H4 protein, human); 0 (hook1 protein, human); 9002-67-9 (Luteinizing Hormone); 9002-68-0 (Follicle Stimulating Hormone); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinase Catalytic Subunits); EC 2.7.11.11 (PRKACB protein, human); EC 3.1.- (CNOT6L protein, human); EC 3.1.- (Ribonucleases); EC 3.6.1.- (Myosin Type I)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-17-0702


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[PMID]:29244110
[Au] Autor:Jamaluddin MFB; Ko YA; Kumar M; Brown Y; Bajwa P; Nagendra PB; Skerrett-Byrne DA; Hondermarck H; Baker MA; Dun MD; Scott RJ; Nahar P; Tanwar PS
[Ad] Endereço:School of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan, New South Wales, Australia.
[Ti] Título:Proteomic Profiling of Human Uterine Fibroids Reveals Upregulation of the Extracellular Matrix Protein Periostin.
[So] Source:Endocrinology;159(2):1106-1118, 2018 02 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The central characteristic of uterine fibroids is excessive deposition of extracellular matrix (ECM), which contributes to fibroid growth and bulk-type symptoms. Despite this, very little is known about patterns of ECM protein expression in fibroids and whether these are influenced by the most common genetic anomalies, which relate to MED12. We performed extensive genetic and proteomic analyses of clinically annotated fibroids and adjacent normal myometrium to identify the composition and expression patterns of ECM proteins in MED12 mutation-positive and mutation-negative uterine fibroids. Genetic sequencing of tissue samples revealed MED12 alterations in 39 of 65 fibroids (60%) from 14 patients. Using isobaric tagged-based quantitative mass spectrometry on three selected patients (n = 9 fibroids), we observed a common set of upregulated (>1.5-fold) and downregulated (<0.66-fold) proteins in small, medium, and large fibroid samples of annotated MED12 status. These two sets of upregulated and downregulated proteins were the same in all patients, regardless of variations in fibroid size and MED12 status. We then focused on one of the significant upregulated ECM proteins and confirmed the differential expression of periostin using western blotting and immunohistochemical analysis. Our study defined the proteome of uterine fibroids and identified that increased ECM protein expression, in particular periostin, is a hallmark of uterine fibroids regardless of MED12 mutation status. This study sets the foundation for further investigations to analyze the mechanisms regulating ECM overexpression and the functional role of upregulated ECM proteins in leiomyogenesis.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/metabolismo
Leiomioma/metabolismo
Proteoma/análise
Neoplasias Uterinas/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Moléculas de Adesão Celular/genética
Transformação Celular Neoplásica/genética
Transformação Celular Neoplásica/metabolismo
Proteínas da Matriz Extracelular/genética
Proteínas da Matriz Extracelular/metabolismo
Feminino
Perfilação da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Leiomioma/genética
Meia-Idade
Miométrio/metabolismo
Proteoma/metabolismo
Proteômica
Neoplasias Uterinas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (Extracellular Matrix Proteins); 0 (POSTN protein, human); 0 (Proteome)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-03018


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[PMID]:27771726
[Au] Autor:Obi AT; Andraska E; Kanthi Y; Luke CE; Elfline M; Madathilparambil S; Siahaan TJ; Jaffer FA; Wakefield TW; Raghavendran K; Henke PK
[Ad] Endereço:Conrad Jobst Vascular Research Laboratory, University of Michigan Medical School, Ann Arbor, Mich., USA.
[Ti] Título:Gram-Negative Pneumonia Alters Large-Vein Cell-Adhesion Molecule Profile and Potentiates Experimental Stasis Venous Thrombosis.
[So] Source:J Vasc Res;53(3-4):186-195, 2016.
[Is] ISSN:1423-0135
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Pneumonia is a significant risk factor for the development of venous thrombosis (VT). Cell-adhesion molecules (CAMs) are linked to the pathogenesis of both pneumonia and VT. We hypothesized that remote infection would confer a prothrombogenic milieu via systemic elevation of CAMs. METHODS: Lung injury was induced in wild-type (C57BL/6) mice by lung contusion or intratracheal inoculation with Klebsiella pneumoniae or saline controls. K. pneumoniae-treated mice and controls additionally underwent inferior vena cava (IVC) ligation to generate VT. RESULTS: Lung-contusion mice demonstrated no increase in E-selectin or P-selectin whereas mice infected with K. pneumoniae demonstrated increased circulating P-selectin, ICAM-1, VCAM-1 and thrombin-antithrombin (TAT) complexes. Mice with pneumonia formed VT 3 times larger than controls, demonstrated significantly more upregulation of vein-wall and systemic CAMs, and formed erythrocyte-rich thrombi. CONCLUSION: Elevated CAM expression was identified in mice with pneumonia, but not lung contusion, indicating that the type of inflammatory stimulus and the presence of infection drive the vein-wall response. Elevation of CAMs was associated with amplified VT and may represent an alternate mechanism by which to target the prevention of VT.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/sangue
Infecções por Klebsiella/complicações
Klebsiella pneumoniae/patogenicidade
Pneumonia Bacteriana/complicações
Veia Cava Inferior/metabolismo
Trombose Venosa/etiologia
[Mh] Termos MeSH secundário: Lesão Pulmonar Aguda/sangue
Lesão Pulmonar Aguda/complicações
Animais
Antitrombina III
Moléculas de Adesão Celular/antagonistas & inibidores
Modelos Animais de Doenças
Fibrinolíticos/farmacologia
Molécula 1 de Adesão Intercelular/sangue
Infecções por Klebsiella/sangue
Infecções por Klebsiella/tratamento farmacológico
Infecções por Klebsiella/microbiologia
Ligadura
Masculino
Camundongos Endogâmicos C57BL
Selectina-P/sangue
Peptídeo Hidrolases/sangue
Pneumonia Bacteriana/sangue
Pneumonia Bacteriana/tratamento farmacológico
Pneumonia Bacteriana/microbiologia
Regulação para Cima
Molécula 1 de Adesão de Célula Vascular/sangue
Veia Cava Inferior/cirurgia
Trombose Venosa/sangue
Trombose Venosa/microbiologia
Trombose Venosa/prevenção & controle
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (Fibrinolytic Agents); 0 (Icam1 protein, mouse); 0 (P-Selectin); 0 (Vascular Cell Adhesion Molecule-1); 0 (antithrombin III-protease complex); 126547-89-5 (Intercellular Adhesion Molecule-1); 9000-94-6 (Antithrombin III); EC 3.4.- (Peptide Hydrolases)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:29225169
[Au] Autor:Yu BX; Yuan JN; Zhang FR; Liu YY; Zhang TT; Li K; Lv XF; Zhou JG; Huang LY; Shang JY; Liang SJ
[Ad] Endereço:Department of Pharmacology, Cardiac and Cerebral Vascular Research Center, Zhongshan School of Medicine, Guangzhou, China; Center for Translational Medicine, The First Affiliated Hospital, Guangzhou, China.
[Ti] Título:Inhibition of Orai1-mediated Ca entry limits endothelial cell inflammation by suppressing calcineurin-NFATc4 signaling pathway.
[So] Source:Biochem Biophys Res Commun;495(2):1864-1870, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Orai1-dependent Ca entry plays an essential role in inflammatory response through regulating T cell and macrophage activation and neutrophil infiltration. However, whether Orai1 Ca entry contributes to endothelial activation, one of the early steps of vascular inflammation, remains elusive. In the present study, we observed that knockdown of Orai1 reduced, whereas overexpression of Orai1 potentiated, TNFα-induced expression of adhesion molecules such as ICAM-1 and VCAM-1 in HUVECs, and subsequently blocked adhesion of monocyte to HUVECs. In vivo, Orai1 downregulation attenuated TNFα-induced ICAM-1 and VCAM-1 expression in mouse aorta and the levels of pro-inflammatory cytokines in the serum. In addition, Orai1 knockdown also dramatically decreased the expression of pro-inflammatory cytokines and neutrophil infiltration in the lung after TNFα treatment, and thus protected lung tissue injury. Notably, among all isoforms of nuclear factor of activated T cells (NFATs), TNFα only triggered NFATc4 nuclear accumulation in HUVECs. Knockdown of Orai1 or inhibition of calcineurin prevented TNFα-induced NFATc4 nuclear translocation and reduced ICAM-1 and VCAM-1 expression in HUVECs. Overexpression of NFATc4 further enhanced ICAM-1 and VCAM-1 expression induced by TNFα. Our study demonstrates that Orai1-Ca -calcineurin-NFATc4 signaling is an essential inflammatory pathway required for TNFα-induced endothelial cell activation and vascular inflammation. Therefore, Orai1 may be a potential therapeutic target for treatment of inflammatory diseases.
[Mh] Termos MeSH primário: Aortite/imunologia
Calcineurina/imunologia
Cálcio/imunologia
Moléculas de Adesão Celular/imunologia
Endotélio Vascular/imunologia
Fatores de Transcrição NFATC/imunologia
Proteína ORAI1/imunologia
[Mh] Termos MeSH secundário: Animais
Aortite/patologia
Células Cultivadas
Regulação para Baixo/imunologia
Seres Humanos
Mediadores da Inflamação/imunologia
Redes e Vias Metabólicas/imunologia
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (Inflammation Mediators); 0 (NFATC Transcription Factors); 0 (Nfatc4 protein, mouse); 0 (ORAI1 Protein); 0 (Orai1 protein, mouse); EC 3.1.3.16 (Calcineurin); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE


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[PMID]:27776343
[Au] Autor:Fradet A; Bouchet M; Delliaux C; Gervais M; Kan C; Benetollo C; Pantano F; Vargas G; Bouazza L; Croset M; Bala Y; Leroy X; Rosol TJ; Rieusset J; Bellahcène A; Castronovo V; Aubin JE; Clézardin P; Duterque-Coquillaud M; Bonnelye E
[Ad] Endereço:InsermUMR1033, F-69372 Lyon, France.
[Ti] Título:Estrogen related receptor alpha in castration-resistant prostate cancer cells promotes tumor progression in bone.
[So] Source:Oncotarget;7(47):77071-77086, 2016 11 22.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bone metastases are one of the main complications of prostate cancer and they are incurable. We investigated whether and how estrogen receptor-related receptor alpha (ERRα) is involved in bone tumor progression associated with advanced prostate cancer. By meta-analysis, we first found that ERRα expression is correlated with castration-resistant prostate cancer (CRPC), the hallmark of progressive disease. We then analyzed tumor cell progression and the associated signaling pathways in gain-of-function/loss-of-function CRPC models in vivo and in vitro. Increased levels of ERRα in tumor cells led to rapid tumor progression, with both bone destruction and formation, and direct impacts on osteoclasts and osteoblasts. VEGF-A, WNT5A and TGFß1 were upregulated by ERRα in tumor cells and all of these factors also significantly and positively correlated withERRα expression in CRPC patient specimens. Finally, high levels of ERRα in tumor cells stimulated the pro-metastatic factor periostin expression in the stroma, suggesting that ERRα regulates the tumor stromal cell microenvironment to enhance tumor progression. Taken together, our data demonstrate that ERRα is a regulator of CRPC cell progression in bone. Therefore, inhibiting ERRα may constitute a new therapeutic strategy for prostate cancer skeletal-related events.
[Mh] Termos MeSH primário: Neoplasias Ósseas/metabolismo
Neoplasias Ósseas/secundário
Neoplasias de Próstata Resistentes à Castração/metabolismo
Receptores Estrogênicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Neoplasias Ósseas/genética
Moléculas de Adesão Celular/metabolismo
Linhagem Celular Tumoral
Progressão da Doença
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Masculino
Camundongos
Transplante de Neoplasias
Neoplasias de Próstata Resistentes à Castração/genética
Receptores Estrogênicos/genética
Transdução de Sinais
Fator de Crescimento Transformador beta1/metabolismo
Microambiente Tumoral
Fator A de Crescimento do Endotélio Vascular/metabolismo
Proteína Wnt-5a/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (ERRalpha estrogen-related receptor); 0 (POSTN protein, human); 0 (Receptors, Estrogen); 0 (TGFB1 protein, human); 0 (Transforming Growth Factor beta1); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); 0 (WNT5A protein, human); 0 (Wnt-5a Protein)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.12787


  9 / 28989 MEDLINE  
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[PMID]:29368829
[Au] Autor:Barkhash AV; Babenko VN; Voevoda MI; Romaschenko AG
[Ti] Título:[Polymorphism of CD209 and TLR3 genes in populations of North Eurasia].
[So] Source:Genetika;52(6):697-704, 2016 Jun.
[Is] ISSN:0016-6758
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:The DC-SIGN (dendritic cell-specific intercellular adhesion molecule (ICAM)-3-grabbing non-integrin) and TLR3 (toll-like receptor 3) proteins are key effectors of the innate immunity and particularly play an important role in the organism's antiviral defense as pattern-recognition receptors. Previously, we demonstrated that certain genotypes and alleles of single nucleotide polymorphisms (SNPs) rs2287886 (G/A) in the promoter region of the CD209 gene (encoding DC-SIGN) and rs3775291 (G/A, Leu412Phe) in the exon 4 of the TLR3 gene are associated with human predisposition to tick-borne encephalitis in the Russian population. In the present work, the distribution of genotype and allele frequencies for these SNPs was studied in seven populations of North Eurasia, including Caucasians (Russians and Germans (from Altai region)), Central Asian Mongoloids (Altaians, Khakass, Tuvinians, and Shorians), and Arctic Mongoloids (Chukchi). It was found that the CD209 gene rs2287886 SNP A/A genotype and A allele, as well as the TLR3 gene rs3775291 SNP G/G genotype and G allele (the frequencies of which in our previous studies were increased in tick-borne encephalitis patients as compared with the population control (Russian citizens of Novosibirsk)), are preserved with a high frequency in Central Asian Mongoloids (who for a long time regularly came in contact with tick-borne encephalitis virus in places of their habitation). We suggested that predisposition to tick-borne encephalitis in Central Asian Mongoloid populations can be predetermined by a different set of genes and their polymorphisms than in the Russian population.
[Mh] Termos MeSH primário: Alelos
Moléculas de Adesão Celular/genética
Genótipo
Lectinas Tipo C/genética
Polimorfismo de Nucleotídeo Único
Receptores de Superfície Celular/genética
Receptor 3 Toll-Like/genética
[Mh] Termos MeSH secundário: Encefalite Transmitida por Carrapatos/genética
Feminino
Seres Humanos
Masculino
Sibéria/etnologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (DC-specific ICAM-3 grabbing nonintegrin); 0 (Lectins, C-Type); 0 (Receptors, Cell Surface); 0 (TLR3 protein, human); 0 (Toll-Like Receptor 3)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE


  10 / 28989 MEDLINE  
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Fotocópia
[PMID]:29283236
[Au] Autor:Kuznik BI; Linkova NS; Kolchina NV; Kukanova EO; Khavinson VK
[Ti] Título:The JAM Family of Molecules and Their Role in the Regulation of Physiological and Pathological Processes.
[So] Source:Usp Fiziol Nauk;47(4):76-97, 2016 Oct-Dec.
[Is] ISSN:0301-1798
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:The review covers the main functions of the family of adhesion molecules JAMs (Junctional adhesion molecules). This review provides information about the role of the molecules JAM-AH, JAM-BH and JAM-CF in the occurrence of pathological conditions, including diseases of the nervous and cardiovascular systems, atherosclerosis, thrombosis and malignant growth. A molecule JAM-C and JAM-C directly affect platelet's adhesion to endothelial and dendritic cells, neutrophils, and other types of leukocytes, which makes their involvement in the regulation of hemostasis, and migration processes. JAM-A has an effect on the inflammatory response, leading to impaired cognitive function in HIV infection. JAM-B is involved in suppression of tumor growth in patients with Down syndrome. It is described the role of molecule JAM-A and JAM-C in the pathogenesis of hypertension, hypertensive crisis, atherosclerosis, cardiac abnormalities in the syndrome of Jacobson. Molecules JAM-B and JAM-C reduce the growth and invasion of human gliomas, and JAM-A has static effect against breast cancer. JAM-A molecule, JAM-B and JAM-C are involved in the development of inflammatory reactions and pathological neoangiogenesis in the cornea. The molecule JAM-C is involved in differentiation and polarization photoreceptors of the retina. The review provides own data of the authors, suggests the presence of epigenetic mechanisms of regulation of expression of the family of molecules JAMs, carried out with the direct participation of peptide geroprotectors.
[Mh] Termos MeSH primário: Plaquetas/metabolismo
Moléculas de Adesão Celular/genética
Epigênese Genética
Receptores de Superfície Celular/genética
[Mh] Termos MeSH secundário: Animais
Plaquetas/patologia
Doenças Cardiovasculares/genética
Doenças Cardiovasculares/metabolismo
Doenças Cardiovasculares/fisiopatologia
Adesão Celular
Moléculas de Adesão Celular/metabolismo
Neovascularização da Córnea/genética
Neovascularização da Córnea/metabolismo
Neovascularização da Córnea/fisiopatologia
Células Endoteliais/metabolismo
Células Endoteliais/patologia
Seres Humanos
Leucócitos/metabolismo
Leucócitos/patologia
Neoplasias/genética
Neoplasias/metabolismo
Neoplasias/fisiopatologia
Doenças do Sistema Nervoso/genética
Doenças do Sistema Nervoso/metabolismo
Doenças do Sistema Nervoso/fisiopatologia
Receptores de Superfície Celular/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (F11R protein, human); 0 (IGSF5 protein, human); 0 (JAM2 protein, human); 0 (JAM3 protein, human); 0 (Receptors, Cell Surface)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171229
[St] Status:MEDLINE



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