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[PMID]:28461624
[Au] Autor:Saleheen D; Zhao W; Young R; Nelson CP; Ho W; Ferguson JF; Rasheed A; Ou K; Nurnberg ST; Bauer RC; Goel A; Do R; Stewart AFR; Hartiala J; Zhang W; Thorleifsson G; Strawbridge RJ; Sinisalo J; Kanoni S; Sedaghat S; Marouli E; Kristiansson K; Hua Zhao J; Scott R; Gauguier D; Shah SH; Smith AV; van Zuydam N; Cox AJ; Willenborg C; Kessler T; Zeng L; Province MA; Ganna A; Lind L; Pedersen NL; White CC; Joensuu A; Edi Kleber M; Hall AS; März W; Salomaa V; O'Donnell C; Ingelsson E; Feitosa MF; Erdmann J; Bowden DW; Palmer CNA; Gudnason V; Faire U
[Ad] Endereço:From Department of Biostatistics and Epidemiology, University of Pennsylvania, Philadelphia (D.S., W.Z.); Center for Non-Communicable Diseases, Karachi, Pakistan (D.S., A.R., P.M.F., PROMIS); Department of Public Health and Primary Care, University of Cambridge, United Kingdom (R.Y., W.K.H., EPIC-CV
[Ti] Título:Loss of Cardioprotective Effects at the Locus as a Result of Gene-Smoking Interactions.
[So] Source:Circulation;135(24):2336-2353, 2017 Jun 13.
[Is] ISSN:1524-4539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Common diseases such as coronary heart disease (CHD) are complex in etiology. The interaction of genetic susceptibility with lifestyle factors may play a prominent role. However, gene-lifestyle interactions for CHD have been difficult to identify. Here, we investigate interaction of smoking behavior, a potent lifestyle factor, with genotypes that have been shown to associate with CHD risk. METHODS: We analyzed data on 60 919 CHD cases and 80 243 controls from 29 studies for gene-smoking interactions for genetic variants at 45 loci previously reported to be associated with CHD risk. We also studied 5 loci associated with smoking behavior. Study-specific gene-smoking interaction effects were calculated and pooled using fixed-effects meta-analyses. Interaction analyses were declared to be significant at a value of <1.0×10 (Bonferroni correction for 50 tests). RESULTS: We identified novel gene-smoking interaction for a variant upstream of the gene. Every T allele of rs7178051 was associated with lower CHD risk by 12% in never-smokers ( =1.3×10 ) in comparison with 5% in ever-smokers ( =2.5×10 ), translating to a 60% loss of CHD protection conferred by this allelic variation in people who smoked tobacco (interaction value=8.7×10 ). The protective T allele at rs7178051 was also associated with reduced expression in human aortic endothelial cells and lymphoblastoid cell lines. Exposure of human coronary artery smooth muscle cells to cigarette smoke extract led to induction of CONCLUSIONS: Allelic variation at rs7178051 that associates with reduced expression confers stronger CHD protection in never-smokers than in ever-smokers. Increased vascular expression may contribute to the loss of CHD protection in smokers.
[Mh] Termos MeSH primário: Doença das Coronárias/genética
Doença das Coronárias/prevenção & controle
Loci Gênicos/genética
Predisposição Genética para Doença/genética
Fumar/genética
[Mh] Termos MeSH secundário: Proteína ADAMTS7/genética
Adulto
Idoso
Idoso de 80 Anos ou mais
Células Cultivadas
Doença das Coronárias/epidemiologia
Vasos Coronários/patologia
Vasos Coronários/fisiologia
Feminino
Interação Gene-Ambiente
Predisposição Genética para Doença/epidemiologia
Seres Humanos
Masculino
Meia-Idade
Polimorfismo de Nucleotídeo Único/genética
Fumar/efeitos adversos
Fumar/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.4.24.- (ADAMTS7 Protein); EC 3.4.24.- (ADAMTS7 protein, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180110
[Lr] Data última revisão:
180110
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCULATIONAHA.116.022069


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[PMID]:28092973
[Au] Autor:Wirtwein M; Melander O; Sjogren M; Hoffmann M; Narkiewicz K; Gruchala M; Sobiczewski W
[Ad] Endereço:a Department of Pharmacology , Medical University of Gdansk , Gdansk , Poland.
[Ti] Título:Elevated ambulatory systolic-diastolic pressure regression index is genetically determined in hypertensive patients with coronary heart disease.
[So] Source:Blood Press;26(3):174-180, 2017 Jun.
[Is] ISSN:1651-1999
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Ambulatory systolic-diastolic pressure regression index (ASDPRI) as a composite marker of cardiovascular (CV) properties is related to CV complications. However, genetic determinants of ASDPRI are not known. The aim of this study is to report the relationship between certain single nucleotide polymorphisms (SNP) and ASDPRI in hypertensive patients with CAD confirmed by coronary angiography. METHODS: A total of 1345 hypertensive subjects with CAD were included. SNPs were selected from genome-wide association studies. SNPs were reported to be associated with coronary artery disease risk. There were significant differences in 24 h and daytime and nighttime ASDPRIs for PHCTR1, LPA and ADAMTS7 polymorphisms. Genetic risk score (GRS18) was constructed to evaluate additive effect of 18 SNPs for ASDPRI. RESULTS: Analysis of covariance revealed a significant relationship between the PPAB2B (ß - 0.85; 95 CI -1.85--0.16, p < 0.02), WDR12 (ß - 1.31; 95 CI -2.19--0.43, p < 0.01) polymorphisms and nighttime ASDPRI dipping. Analysis of covariance revealed a significant relationship between GRS 18 and 24-h ASDPRI (ß 0.34; 95 CI 0.16-0.31, p < 0.01). CONCLUSIONS: In conclusion, ADAMTS7 and LPA polymorphisms are related to 24-h ASDPRI but PPAB2B and WDR12 gene polymorphisms are associated with nighttime ASDPRI dipping. A total of 24-h ASDPRI is determined by GRS18.
[Mh] Termos MeSH primário: Pressão Sanguínea
Doença das Coronárias/genética
Hipertensão/genética
Polimorfismo de Nucleotídeo Único
Receptores de Ácidos Lisofosfatídicos/genética
[Mh] Termos MeSH secundário: Proteína ADAMTS7/genética
Idoso
Monitorização Ambulatorial da Pressão Arterial
Ritmo Circadiano
Doença das Coronárias/complicações
Doença das Coronárias/fisiopatologia
Diástole
Feminino
Expressão Gênica
Estudo de Associação Genômica Ampla
Seres Humanos
Hipertensão/complicações
Hipertensão/fisiopatologia
Masculino
Meia-Idade
Projetos de Pesquisa
Estudos Retrospectivos
Risco
Sístole
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Lysophosphatidic Acid); EC 3.4.24.- (ADAMTS7 Protein); EC 3.4.24.- (ADAMTS7 protein, human)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170302
[Lr] Data última revisão:
170302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170118
[St] Status:MEDLINE
[do] DOI:10.1080/08037051.2016.1273741


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[PMID]:27902619
[Au] Autor:Yu J; Zhou B; Yu H; Han J; Cui M; Zhang F; Wang G; Guo L; Gao W
[Ad] Endereço:Department of Cardiology, Peking University Third Hospital, Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Ministry of Health, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing, China.
[Ti] Título:Association between plasma ADAMTS-7 levels and severity of disease in patients with stable obstructive coronary artery disease.
[So] Source:Medicine (Baltimore);95(48):e5523, 2016 Nov.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The metalloproteinase family of a disintegrin and metalloproteinase with thrombospondin motifs-7 (ADAMTS-7) was reported to be a novel locus associated with human coronary artery disease. This study aimed to investigate plasma ADAMTS-7 levels in stable obstructive CAD patients and elucidate the relationship between plasma ADAMTS-7 levels and the severity of CAD assessed by the Syntax score.This was a single center cross-sectional study performed in 182 CAD patients. ELISA was used to measure plasma ADAMTS-7 levels. All patients were divided into subgroup according to the ADAMTS-7 median in this cohort: high group with ADAMTS-7 ≥0.99 ng/mL and low group with ADAMTS-7 <0.99 ng/mL. Furthermore, all patients were divided into tertiles according to their Syntax scores (low group: Syntax score ≤10.0; moderate group: 10.0 18.0). We followed up the participants continuously until the first major adverse cardiovascular event (MACE) for a mean time of 22.0 months.Plasma ADAMTS-7 levels in the high Syntax score group were significantly higher compared with the low Syntax score group (3.29 [0.08-26.3] ng/mL vs 1.24 [0.15-8.78] ng/mL, P = 0.010). Plasma ADAMTS-7 levels were significantly positively correlated with the Syntax score tertiles (r = 0.157, P = 0.035). Logistic regression analysis indicated that the plasma ADAMTS-7 level was one of the independent predictors for the Syntax score tertiles (B = 1.118, 95% CI: 1.194-7.830, P = 0.020), together with HbA1c (B = 0.946, 95% CI: 1.248-5.312, P = 0.010), uric acid (B = -0.019, 95% CI: 0.974-0.988, P<0.001), and coronary artery calcium score (B = -0.001, 95% CI: 0.998-0.999, P < 0.001). Compared with the low ADAMTS-7 group, the high ADAMTS-7 group had significantly higher Syntax score (17.10±8.42 vs 14.96 ±â€Š8.11, P = 0.047). Kaplan-Meier analysis showed patients in the high plasma ADAMTS-7 group tend to have a lower event-free survival rate than patients in the low plasma ADAMTS-7 group, unfortunately, no difference was detected (86.8% vs 88.0%, log rank = 0.314, P = 0.575).The plasma ADAMTS-7 level was positively correlated with the Syntax score significantly. The elevated plasma ADAMTS-7 level may be involved in the severity of disease in patients with stable coronary artery disease.
[Mh] Termos MeSH primário: Proteína ADAMTS7/sangue
Doença da Artéria Coronariana/sangue
Índice de Gravidade de Doença
[Mh] Termos MeSH secundário: Idoso
Angiografia Coronária
Doença da Artéria Coronariana/diagnóstico por imagem
Estudos Transversais
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Masculino
Meia-Idade
Estudos Retrospectivos
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.4.24.- (ADAMTS7 Protein)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170224
[Lr] Data última revisão:
170224
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161201
[St] Status:MEDLINE


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[PMID]:27516213
[Au] Autor:Wang X; Li C; Liang A; Peng Y; Sun J; Huang D; Xu K; Ye W
[Ad] Endereço:Department of Spine Surgery, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Yan Jiang Xi RD 107, Guangzhou, 510120, China.
[Ti] Título:Regulation of a disintegrins and metalloproteinase with thrombospondin motifs 7 during inflammation in nucleus pulposus (NP) cells: role of AP-1, Sp1 and NF-κB signaling.
[So] Source:Inflamm Res;65(12):951-962, 2016 Dec.
[Is] ISSN:1420-908X
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:AIM: The objective of this study is to explore the effect of inflammatory cytokines on a disintegrins and metalloproteinase with thrombospondin motifs 7 (ADAMTS7) and to demonstrate the role of Sp1, AP-1 and NF-κB signaling on the ADAMTS7 regulation during inflammation in NP cells. METHODS: Real-time PCR was to detect the effect of ADAMTS7 knockdown on the expression of catabolic enzymes during inflammatory condition in NP cells. Real-time PCR, western blot, immunofluorescence and transfection experiments were used to observe the effect of tumor necrosis factor-α (TNF-α) or interleukin-1ß on the expression and the activity of ADAMTS7, and demonstrated the role to Sp1, AP-1 and NF-κB in the regulation of ADAMTS7 during inflammation. RESULTS: As other cells, ADAMTS7 knockdown suppressed the mRNA expression of catabolic factors during inflammation in human NP cells. However, the expression of ADAMTS7 mRNA and protein and the activity of ADAMTS7 promoter were refractory to inflammatory cytokines. In addition, Sp1, AP-1, not NF-κB signaling sustained the expression of ADAMTS7 mRNA, protein, as well as promoter activity during inflammation in NP cells. CONCLUSION: ADAMTS7 played a crucial role in the expression of catabolic genes in the presence of TNF-α and AP-1, Sp1, not NF-κB signaling were critical for the maintenance of ADAMTS7 expression during inflammation in NP cells.
[Mh] Termos MeSH primário: Inflamação/metabolismo
Núcleo Pulposo/citologia
Fator de Transcrição AP-1/metabolismo
[Mh] Termos MeSH secundário: Proteína ADAMTS7/genética
Proteína ADAMTS7/metabolismo
Animais
Benzamidas/farmacologia
Diterpenos Abietanos/farmacologia
Células HEK293
Seres Humanos
Inflamação/genética
NF-kappa B/antagonistas & inibidores
NF-kappa B/metabolismo
Ratos
Fator de Transcrição Sp1/genética
Fator de Transcrição Sp1/metabolismo
Tiazóis/farmacologia
Fator de Transcrição AP-1/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzamides); 0 (Diterpenes, Abietane); 0 (NF-kappa B); 0 (SM 7368); 0 (Sp1 Transcription Factor); 0 (Thiazoles); 0 (Transcription Factor AP-1); 03UUH3J385 (tanshinone); EC 3.4.24.- (ADAMTS7 Protein); EC 3.4.24.- (ADAMTS7 protein, human)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170916
[Lr] Data última revisão:
170916
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160813
[St] Status:MEDLINE


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[PMID]:26938210
[Au] Autor:Wu W; Wang H; Yu C; Li J; Gao Y; Ke Y; Wang Y; Zhou Y; Zheng J
[Ad] Endereço:Department of Cardiology, China-Japan Friendship Hospital, Beijing, Beijing, China.
[Ti] Título:Association of ADAMTS-7 Levels with Cardiac Function in a Rat Model of Acute Myocardial Infarction.
[So] Source:Cell Physiol Biochem;38(3):950-8, 2016.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: High ADAMTS-7 levels are associated with acute myocardial infarction (AMI), although its involvement in ventricular remodeling is unclear. In this study, we investigated the association between ADAMTS-7 expression and cardiac function in a rat AMI model. METHODS: Sprague-Dawley rats were randomized into AMI (n = 40) and sham (n = 20) groups. The left anterior descending artery was sutured to model AMI. Before surgery and 7, 14, 28, and 42 days post-surgery, ADAMTS-7 and brain natriuretic peptide (BNP), and cartilage oligomeric matrix protein (COMP) were assessed by ELISA, western blot, real-time RT-PCR, and/or immunohistochemistry. Cardiac functional and structural parameters were assessed by M-mode echocardiography. RESULTS: After AMI, plasma ADAMTS-7 levels increased, peaking on day 28 (AMI: 13.2 ± 6.3 vs. sham: 3.4 ± 1.3 ng/ml, P < 0.05). Compared with the sham group, ADAMTS-7 expression was higher in the infarct zone at day 28. COMP present in normal myocardium was degraded by day 28 post-AMI. Plasma ADAMTS-7 correlated positively with BNP (r = 0.642, P = 0.025), left ventricular end-diastolic diameter (r = 0.695, P = 0.041), left ventricular end-systolic diameter (r = 0.710, P = 0.039), left ventricular ejection fraction (r = 0.695, P = 0.036), and left ventricular short-axis fractional shortening (r = 0.721, P = 0.024). CONCLUSIONS: ADAMTS-7 levels may reflect the degree of ventricular remodeling after AMI.
[Mh] Termos MeSH primário: Proteína ADAMTS7/sangue
Proteína ADAMTS7/genética
Infarto do Miocárdio/fisiopatologia
Função Ventricular Esquerda
Remodelação Ventricular
[Mh] Termos MeSH secundário: Animais
Proteína de Matriz Oligomérica de Cartilagem/genética
Proteína de Matriz Oligomérica de Cartilagem/metabolismo
Modelos Animais de Doenças
Ecocardiografia
Masculino
Infarto do Miocárdio/genética
Infarto do Miocárdio/metabolismo
Peptídeo Natriurético Encefálico/genética
Peptídeo Natriurético Encefálico/metabolismo
Distribuição Aleatória
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (COMP protein, rat); 0 (Cartilage Oligomeric Matrix Protein); 0 (natriuretic peptide precursor type B, rat); 114471-18-0 (Natriuretic Peptide, Brain); EC 3.4.24.- (ADAMTS7 Protein); EC 3.4.24.- (Adamts7 protein, rat)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160304
[St] Status:MEDLINE
[do] DOI:10.1159/000443047


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[PMID]:26872430
[Au] Autor:Müller M; Kessler T; Schunkert H; Erdmann J; Tennstedt S
[Ad] Endereço:Institut für Integrative und Experimentelle Genomik, Universität zu Lübeck, Maria-Goeppert-Str. 1, 23562 Lübeck, Germany; DZHK (German Centre for Cardiovascular Research), Partner Site Hamburg/Lübeck/Kiel, Germany; University Heart Center Luebeck, 23562 Lübeck, Germany.
[Ti] Título:Classification of ADAMTS binding sites: The first step toward selective ADAMTS7 inhibitors.
[So] Source:Biochem Biophys Res Commun;471(3):380-5, 2016 Mar 11.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Genome-wide association studies identified ADAMTS7 as a risk locus for coronary artery disease. In carotid arteries of rats, neointima formation after balloon-mediated injury goes along with enhanced Adamts7 expression. Vice versa, Adamts7-deficient mice display reduced neointima formation following vascular injury. Although a causal link between ADAMTS7 and coronary artery disease remains to be proven, inhibition of ADAMTS7 represents a potential new target for intervention in this disease. ADAMTS7, a member of the 'a disintegrin and metalloproteinase with thrombospondin motifs' (ADAMTS) family of proteins, contains a catalytic zinc ion in the binding site of its metalloproteinase domain. The structure of ADAMTS7 and its inhibitors are unknown. In this study, we used in silico methods, including homology modeling and pharmacophore modeling, to analyze the ADAMTS7 metalloproteinase domain, particularly its binding site. The results revealed structural and sequence differences relative to the binding sites of the other ADAMTS proteins; these non-conserved regions represent potential binding regions for selective ADAMTS7 inhibitors. The main contribution of this study is the proposal of a pharmacophore for ADAMTS7. The characterization of the ADAMTS7 binding site and definition of a pharmacophore are the first step toward developing a new therapeutic target for coronary artery disease.
[Mh] Termos MeSH primário: Proteínas ADAM/química
Proteínas ADAM/ultraestrutura
Modelos Químicos
Simulação de Acoplamento Molecular
Análise de Sequência de Proteína/métodos
[Mh] Termos MeSH secundário: Proteína ADAMTS7
Sequência de Aminoácidos
Sítios de Ligação
Sequência Conservada
Ativação Enzimática
Inibidores Enzimáticos/química
Dados de Sequência Molecular
Ligação Proteica
Estrutura Terciária de Proteína
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Enzyme Inhibitors); EC 3.4.24.- (ADAM Proteins); EC 3.4.24.- (ADAMTS7 Protein); EC 3.4.24.- (ADAMTS7 protein, human)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160214
[St] Status:MEDLINE


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[PMID]:26189211
[Au] Autor:You L; Tan L; Liu L; Shen R; Chaugai S; Wang DW; Cui W
[Ad] Endereço:Division of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, People's Republic of China.
[Ti] Título:ADAMTS7 locus confers high cross-race risk for development of coronary atheromatous plaque.
[So] Source:Mol Genet Genomics;291(1):121-8, 2016 Feb.
[Is] ISSN:1617-4623
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Genome-wide association studies of coronary artery disease (CAD) have recently identified a new susceptibility locus, ADAMTS7, in subjects of European ancestry. However, the significance of this locus in Chinese populations has not been identified. Therefore, this study was designed to evaluate the effect of rs3825807, a non-synonymous variant in the prodomain of the ADAMTS7 protease, on CAD risk and atherosclerosis severity in a Chinese population. We performed genetic association analyses in two independent case-control cohorts, which included a total of 8154 participants. Additionally, the association between the ADAMTS7 rs3825807 genotype and the proportion of CAD patients with 3- and 1-vessel disease was tested. We found that ADAMTS7 rs3825807 was associated with susceptibility to CAD in a Chinese population [odds ratio (OR) = 1.15, 95 % confidence interval (CI) = 1.05-1.26, P = 0.002]. The association remained significant after adjusting for clinical covariates (adjusted OR = 1.12, 95 % CI = 1.02-1.24, P = 0.02). Among 3741 angiographically documented CAD patients, the rs3825807 risk allele showed a significant association with disease severity (P = 0.04, trend P = 0.02). Additionally, 3-vessel disease demonstrated a strong and direct association with ADAMTS7 rs3825807 gene dosage (P = 0.02). Overall, our findings indicate that the significant associations observed between this coding variant in ADAMTS7 and the risk of CAD development are cross-ethnic, and the gene dosage is consistent with the degree of coronary atheromatous burden.
[Mh] Termos MeSH primário: Proteínas ADAM/genética
Doença da Artéria Coronariana/genética
Predisposição Genética para Doença/genética
Placa Aterosclerótica/genética
[Mh] Termos MeSH secundário: Proteína ADAMTS7
Alelos
Grupo com Ancestrais do Continente Asiático/genética
Estudos de Casos e Controles
Feminino
Frequência do Gene/genética
Estudo de Associação Genômica Ampla/métodos
Genótipo
Seres Humanos
Masculino
Meia-Idade
Polimorfismo Genético/genética
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 3.4.24.- (ADAM Proteins); EC 3.4.24.- (ADAMTS7 Protein); EC 3.4.24.- (ADAMTS7 protein, human)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:171007
[Lr] Data última revisão:
171007
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150720
[St] Status:MEDLINE
[do] DOI:10.1007/s00438-015-1092-9


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[PMID]:26696755
[Au] Autor:Zhang Y; Lin J; Wei F
[Ad] Endereço:School of Biological Science and Technology, University of Jinan, Jinan 250022, China.
[Ti] Título:The Function and Roles of ADAMTS-7 in Inflammatory Diseases.
[So] Source:Mediators Inflamm;2015:801546, 2015.
[Is] ISSN:1466-1861
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The ADAMTS proteinases are a group of multidomain and secreted metalloproteinases containing the thrombospondin motifs. ADAMTS-7 is a member of ADAMTS family and plays a crucial role in the pathogenesis of arthritis. Overexpression of ADAMTS-7 gene promotes the breakdown of cartilage oligomeric matrix protein (COMP) matrix and accelerates the progression of both surgically induced osteoarthritis and collagen-induced arthritis. Moreover, ADAMTS-7 and tumor necrosis factor-α (TNF-α) form a positive feedback loop in osteoarthritis. More significantly, granulin-epithelin precursor, a growth factor has important roles in bone development and bone-associated diseases, disturbs the interaction between ADAMTS-7 and COMP, and prevents COMP degradation. This review is based on our results and provides an overview of current knowledge of ADAMTS-7, including its structure, function, gene regulation, and inflammatory diseases involvement.
[Mh] Termos MeSH primário: Proteínas ADAM/fisiologia
Inflamação/etiologia
[Mh] Termos MeSH secundário: Proteínas ADAM/química
Proteínas ADAM/genética
Proteínas ADAMTS
Proteína ADAMTS7
Artrite/etiologia
Aterosclerose/etiologia
Catecol O-Metiltransferase/metabolismo
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
EC 2.1.1.6 (COMT protein, human); EC 2.1.1.6 (Catechol O-Methyltransferase); EC 3.4.24.- (ADAM Proteins); EC 3.4.24.- (ADAMTS Proteins); EC 3.4.24.- (ADAMTS12 protein, human); EC 3.4.24.- (ADAMTS7 Protein); EC 3.4.24.- (ADAMTS7 protein, human)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151224
[St] Status:MEDLINE
[do] DOI:10.1155/2015/801546


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[PMID]:26446668
[Au] Autor:Wang SS; Zhang W; Zhang YQ; Zhao Y; Liu Y; Li JK; Zhang HX; Cheng L; Nie L
[Ad] Endereço:Department of Orthopedics, Qilu Hospital of Shandong University, Jinan, 250012, China.
[Ti] Título:IL-17A enhances ADAMTS-7 expression through regulation of TNF-α in human nucleus pulposus cells.
[So] Source:J Mol Histol;46(6):475-83, 2015 Dec.
[Is] ISSN:1567-2387
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:ADMATS-7 is known to play an important role in the pathogenesis of various diseases, including cartilaginous diseases. IL-17A is an inflammatory cytokine detected in degenerative disc tissues. However, the interplay between IL-17A and ADMATS-7 in human disc degeneration is still unknown. Samples collected from 50 patients were divided into three groups according to MRI degeneration grading system score. Immunohistochemistry, RT-PCR and western Blotting were used to investigate the expression of ADAMTS-7 in NP tissues. Furthermore, a rat disc degeneration model was established, and the expression level of ADAMTS-7 was assayed using immunohistochemistry, RT-PCR and western Blotting. The human NP cells were cultured in the presence and absence of IL-17A stimulation. RNA extracts were collected, and real-time PCR was performed to determine the expression of ADAMTS-7. Moreover, ADAMTS-7 concentrations were detected in human NP cell culture supernatants by ELISA. After culturing NP cells with IL-17A (with or without Etanercept), ADAMTS-7 levels were detected in each group. ADAMTS-7 expression was dramatically elevated in both human and rat degenerative NP tissues compared with normal controls. The RT-PCR and ELISA results revealed that IL-17A could enhance the production of ADAMTS-7, while ADAMTS-7 expression dramatically decreased in the IL-17A + Etanercept group in comparison to the IL-17A alone group. Our results indicate the presence of ADAMTS-7 in human NP cells and imply its potential role in disc degeneration. Additionally, our results indicate that IL-17A induced ADAMTS-7 expression via TNF-α, which may form a molecular axis in human NP cells.
[Mh] Termos MeSH primário: Proteínas ADAM/genética
Expressão Gênica
Interleucina-17/metabolismo
Disco Intervertebral/citologia
Disco Intervertebral/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Proteínas ADAM/metabolismo
Proteína ADAMTS7
Adulto
Idoso
Animais
Modelos Animais de Doenças
Etanercepte/farmacologia
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Imuno-Histoquímica
Interleucina-17/farmacologia
Degeneração do Disco Intervertebral/genética
Degeneração do Disco Intervertebral/metabolismo
Degeneração do Disco Intervertebral/patologia
Masculino
Meia-Idade
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ratos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-17); 0 (RNA, Messenger); 0 (Tumor Necrosis Factor-alpha); EC 3.4.24.- (ADAM Proteins); EC 3.4.24.- (ADAMTS7 Protein); EC 3.4.24.- (ADAMTS7 protein, human); OP401G7OJC (Etanercept)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151009
[St] Status:MEDLINE
[do] DOI:10.1007/s10735-015-9640-5


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[PMID]:26162802
[Au] Autor:Zhang Q; Ji Q; Wang X; Kang L; Fu Y; Yin Y; Li Z; Liu Y; Xu X; Wang Y
[Ad] Endereço:Department of Orthopaedics, The General Hospital of Chinese People's Liberation Army, Beijing 100853, China; Department of Orthopaedic Surgery, Royal Liverpool University Hospital, Prescot Street, Liverpool, UK.
[Ti] Título:SOX9 is a regulator of ADAMTSs-induced cartilage degeneration at the early stage of human osteoarthritis.
[So] Source:Osteoarthritis Cartilage;23(12):2259-2268, 2015 Dec.
[Is] ISSN:1522-9653
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To identify whether cartilage master regulator SRY-related protein 9 (SOX9) mediates A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) dysregulation during osteoarthritis (OA) cartilage degeneration. METHOD: Twenty-two randomly selected OA patients were evaluated using Outerbridge Classification via arthroscopy. Haematoxylin-eosin (HE), Safranin O and Masson staining were performed for the histopathological assessment. The expression of ADAMTSs, collagen 2A1 (COL2A1), aggrecan (ACAN), cartilage oligomeric matrix protein (COMP) and SOX9 were examined using real-time quantitative Polymerase Chain Reaction (PCR) (RT-qPCR) and western blotting analysis. Immunohistochemistry (IHC) analysis was performed to investigate the production of ADAMTSs in cartilage tissues. The association between SOX9 production and ADAMTSs, COL2A1, ACAN, and COMP expression was established by full-depth cartilage biopsies. RESULTS: ADAMTSs expression levels were repressed at stage 1, while a significant increase was observed at the progressive stage of OA. SOX9 was upregulated at stage 1 and suppressed at a later stage of cartilage development, particularly in cartilage with severe damage. In addition, SOX9 repressed the expression of ADAMTSs and promoted COL2A1, ACAN and COMP expression in human chondrocytes. SOX9 was recruited to the promoters of ADAMTS-4 and ADAMTS-7. SOX9 expression was negatively correlated with ADAMTSs production and was positively associated with COL2A1, ACAN and COMP expression. Inhibition of ADAMTSs markedly increased the production of COL2A1, ACAN and COMP in chondrocytes isolated from the early stage of OA. CONCLUSIONS: These findings indicated that SOX9 upregulation might mediate ADAMTSs suppression at the early stage of human OA. In addition, SOX9 could be used as a potential therapeutic agent for human OA at an early stage.
[Mh] Termos MeSH primário: Agrecanas/genética
Proteína de Matriz Oligomérica de Cartilagem/genética
Cartilagem Articular/metabolismo
Condrócitos/metabolismo
Colágeno Tipo II/genética
Osteoartrite do Joelho/genética
Fatores de Transcrição SOX9/genética
[Mh] Termos MeSH secundário: Proteínas ADAM
Proteínas ADAMTS
Proteína ADAMTS4
Proteína ADAMTS5
Proteína ADAMTS7
Agrecanas/metabolismo
Western Blotting
Proteína de Matriz Oligomérica de Cartilagem/metabolismo
Células Cultivadas
Colágeno Tipo II/metabolismo
Feminino
Seres Humanos
Imuno-Histoquímica
Masculino
Meia-Idade
Osteoartrite do Joelho/metabolismo
Pró-Colágeno N-Endopeptidase
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fatores de Transcrição SOX9/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aggrecans); 0 (COL2A1 protein, human); 0 (Cartilage Oligomeric Matrix Protein); 0 (Collagen Type II); 0 (SOX9 Transcription Factor); 0 (SOX9 protein, human); EC 3.4.24.- (ADAM Proteins); EC 3.4.24.- (ADAMTS Proteins); EC 3.4.24.- (ADAMTS12 protein, human); EC 3.4.24.- (ADAMTS5 Protein); EC 3.4.24.- (ADAMTS5 protein, human); EC 3.4.24.- (ADAMTS7 Protein); EC 3.4.24.- (ADAMTS7 protein, human); EC 3.4.24.14 (Procollagen N-Endopeptidase); EC 3.4.24.82 (ADAMTS4 Protein); EC 3.4.24.82 (ADAMTS4 protein, human)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150712
[St] Status:MEDLINE



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