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[PMID]:29079415
[Au] Autor:Boguslawska J; Rodzik K; Poplawski P; Kedzierska H; Rybicka B; Sokól E; Tanski Z; Piekielko-Witkowska A
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Centre of Postgraduate Medical Education, ul. Marymoncka 99/103, 01-813 Warsaw, Poland.
[Ti] Título:TGF-ß1 targets a microRNA network that regulates cellular adhesion and migration in renal cancer.
[So] Source:Cancer Lett;412:155-169, 2018 Jan 01.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:In our previous study we found altered expression of 19 adhesion-related genes in renal tumors. In this study we hypothesized that disturbed expression of adhesion-related genes could be caused by microRNAs: short, non-coding RNAs that regulate gene expression. Here, we found that expression of 24 microRNAs predicted to target adhesion-related genes was disturbed in renal tumors and correlated with expression of their predicted targets. miR-25-3p, miR-30a-5p, miR-328 and miR-363-3p directly targeted adhesion-related genes, including COL5A1, COL11A1, ITGA5, MMP16 and THBS2. miR-363-3p and miR-328 inhibited proliferation of renal cancer cells, while miR-25-3p inhibited adhesion, promoted proliferation and migration of renal cancer cells. TGF-ß1 influenced the expression of miR-25-3p, miR-30a-5p, and miR-328. The analyzed microRNAs, their target genes and TGF-ß1 formed a network of strong correlations in tissue samples from renal cancer patients. The expression signature of microRNAs linked with TGF-ß1 levels correlated with poor survival of renal cancer patients. The results of our study suggest that TGF-ß1 coordinates the expression of microRNA network that regulates cellular adhesion in cancer.
[Mh] Termos MeSH primário: Regulação Neoplásica da Expressão Gênica
Neoplasias Renais/patologia
MicroRNAs/fisiologia
Fator de Crescimento Transformador beta1/fisiologia
[Mh] Termos MeSH secundário: Adesão Celular
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Colágeno Tipo V/genética
Biologia Computacional
Matriz Extracelular/fisiologia
Redes Reguladoras de Genes
Seres Humanos
Integrina alfaV/genética
Neoplasias Renais/genética
Neoplasias Renais/mortalidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (COL5A1 protein, human); 0 (Collagen Type V); 0 (Integrin alphaV); 0 (MicroRNAs); 0 (Transforming Growth Factor beta1)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171205
[Lr] Data última revisão:
171205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171029
[St] Status:MEDLINE


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[PMID]:28734943
[Au] Autor:Park AC; Phan N; Massoudi D; Liu Z; Kernien JF; Adams SM; Davidson JM; Birk DE; Liu B; Greenspan DS
[Ad] Endereço:Department of Cell and Regenerative Biology, University of Wisconsin, Madison, Wisconsin.
[Ti] Título:Deficits in Col5a2 Expression Result in Novel Skin and Adipose Abnormalities and Predisposition to Aortic Aneurysms and Dissections.
[So] Source:Am J Pathol;187(10):2300-2311, 2017 Oct.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Classic Ehlers-Danlos syndrome (cEDS) is characterized by fragile, hyperextensible skin and hypermobile joints. cEDS can be caused by heterozygosity for missense mutations in genes COL5A2 and COL5A1, which encode the α2(V) and α1(V) chains, respectively, of collagen V, and is most often caused by COL5A1 null alleles. However, COL5A2 null alleles have yet to be associated with cEDS or other human pathologies. We previously showed that mice homozygous null for the α2(V) gene Col5a2 are early embryonic lethal, whereas haploinsufficiency caused aberrancies of adult skin, but not a frank cEDS-like phenotype, as skin hyperextensibility at low strain and dermal cauliflower-contoured collagen fibril aggregates, two cEDS hallmarks, were absent. Herein, we show that ubiquitous postnatal Col5a2 knockdown results in pathognomonic dermal cauliflower-contoured collagen fibril aggregates, but absence of skin hyperextensibility, demonstrating these cEDS hallmarks to arise separately from loss of collagen V roles in control of collagen fibril growth and nucleation events, respectively. Col5a2 knockdown also led to loss of dermal white adipose tissue (WAT) and markedly decreased abdominal WAT that was characterized by miniadipocytes and increased collagen deposition, suggesting α2(V) to be important to WAT development/maintenance. More important, Col5a2 haploinsufficiency markedly increased the incidence and severity of abdominal aortic aneurysms, and caused aortic arch ruptures and dissections, indicating that α2(V) chain deficits may play roles in these pathologies in humans.
[Mh] Termos MeSH primário: Tecido Adiposo/anormalidades
Aneurisma da Aorta Torácica/genética
Colágeno Tipo V/deficiência
Colágeno/deficiência
Predisposição Genética para Doença
Anormalidades da Pele/metabolismo
Pele/patologia
[Mh] Termos MeSH secundário: Tecido Adiposo/efeitos dos fármacos
Tecido Adiposo/patologia
Animais
Aneurisma da Aorta Torácica/patologia
Colágeno/metabolismo
Colágeno Tipo V/metabolismo
Derme/patologia
Modelos Animais de Doenças
Síndrome de Ehlers-Danlos/patologia
Colágenos Fibrilares/metabolismo
Deleção de Genes
Técnicas de Silenciamento de Genes
Integrases/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Reprodutibilidade dos Testes
Pele/efeitos dos fármacos
Pele/ultraestrutura
Anormalidades da Pele/patologia
Tamoxifeno/farmacologia
Cicatrização/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Col5a2 protein, mouse); 0 (Collagen Type V); 0 (Fibrillar Collagens); 094ZI81Y45 (Tamoxifen); 9007-34-5 (Collagen); EC 2.7.7.- (Cre recombinase); EC 2.7.7.- (Integrases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170724
[St] Status:MEDLINE


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[PMID]:28618934
[Au] Autor:Li H; Wu H; Zhang H; Li Y; Li S; Hou Q; Wu S; Yang SY
[Ad] Endereço:1 Department of Respiratory Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
[Ti] Título:Identification of curcumin-inhibited extracellular matrix receptors in non-small cell lung cancer A549 cells by RNA sequencing.
[So] Source:Tumour Biol;39(6):1010428317705334, 2017 Jun.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Curcumin is a potent anti-cancer drug in several types of human cancers. Despite of several preclinical and clinical studies of curcumin, the precise mechanism of curcumin in cancer prevention has remained unclear. In our study, we for the first time investigated whole transcriptome alteration in A549 non-small cell lung cancer (NSCLC) cell lines after treatment with curcumin using RNA sequencing. We found that lots of genes and signaling pathways were significantly altered after curcumin treatment in A549 cells. With bioinformatics approaches (gene ontology, Kyoto Encyclopedia of Genes and Genomes, and STRING), we found that those curcumin altered genes were not only the genes that induce cell death but also those extracellular matrix receptors and mitogen-activated protein kinase signaling pathway genes which regulate cell migration and proliferation. Among those significantly altered genes, eight genes ( COL1A1, COL4A1, COL5A1, LAMA5, ITGA3, ITGA2B, DDIT3, and DUSP1) were further examined by quantitative reverse transcription polymerase chain reaction and western blot analysis in four non-small cell lung cancer cell lines. Both in cell lines and in mouse model, the extracellular matrix receptors including the integrin ( ITGA3 and ITGA2B), collagen ( COL5A1), and laminin ( LAMA5) were significantly inhibited by curcumin at messenger RNA and protein levels. Functional studies confirmed that curcumin not only induced A549 cell death but also repressed cell proliferation and migration by regulating extracellular matrix receptors. Collectively, our study suggests that curcumin may be used as a promising drug candidate for intervening lung cancer in future studies.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Colágeno Tipo V/biossíntese
Curcumina/administração & dosagem
Integrina alfa2/biossíntese
Integrina alfa3/biossíntese
Laminina/biossíntese
[Mh] Termos MeSH secundário: Células A549
Animais
Apoptose/efeitos dos fármacos
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma Pulmonar de Células não Pequenas/patologia
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Colágeno Tipo V/genética
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Integrina alfa2/genética
Integrina alfa3/genética
Laminina/genética
Camundongos
RNA Mensageiro/biossíntese
Receptores de Superfície Celular/antagonistas & inibidores
Receptores de Superfície Celular/genética
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (COL5A1 protein, human); 0 (Collagen Type V); 0 (ITGA2B protein, human); 0 (ITGA3 protein, human); 0 (Integrin alpha2); 0 (Integrin alpha3); 0 (Laminin); 0 (RNA, Messenger); 0 (Receptors, Cell Surface); 0 (extracellular matrix receptor); 0 (laminin alpha5); IT942ZTH98 (Curcumin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170718
[Lr] Data última revisão:
170718
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170617
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317705334


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[PMID]:28192633
[Au] Autor:Bowen JM; Sobey GJ; Burrows NP; Colombi M; Lavallee ME; Malfait F; Francomano CA
[Ti] Título:Ehlers-Danlos syndrome, classical type.
[So] Source:Am J Med Genet C Semin Med Genet;175(1):27-39, 2017 Mar.
[Is] ISSN:1552-4876
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Classical EDS is a heritable disorder of connective tissue. Patients are affected with joint hypermobility, skin hyperextensibilty, and skin fragility leading to atrophic scarring and significant bruising. These clinical features suggest consideration of the diagnosis which then needs to be confirmed, preferably by genetic testing. The most recent criteria for the diagnosis of EDS were devised in Villefranche in 1997. [Beighton et al. (1998); Am J Med Genet 77:31-37]. The aims set out in the Villefranche Criteria were: to enable diagnostic uniformity for clinical and research purposes, to understand the natural history of each subtype of EDS, to inform management and genetic counselling, and to identify potential areas of research. The authors recognized that the criteria would need updating, but viewed the Villefranche nosology as a good starting point. Since 1997, there have been major advances in the molecular understanding of classical EDS. Previous question marks over genetic heterogeneity have been largely surpassed by evidence that abnormalities in type V collagen are the cause. Advances in molecular testing have made it possible to identify the causative mutation in the majority of patients. This has aided the further clarification of this diagnosis. The aim of this literature review is to summarize the current knowledge and highlight areas for future research. © 2017 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Síndrome de Ehlers-Danlos/diagnóstico
[Mh] Termos MeSH secundário: Colágeno Tipo V/genética
Síndrome de Ehlers-Danlos/classificação
Testes Genéticos
Seres Humanos
Técnicas de Diagnóstico Molecular
Mutação
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Collagen Type V)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170214
[St] Status:MEDLINE
[do] DOI:10.1002/ajmg.c.31548


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[PMID]:27884590
[Au] Autor:Sturgeon KM; Schweitzer A; Leonard JJ; Tobias DK; Liu Y; Cespedes Feliciano E; Malik VS; Joshi A; Rosner B; De Jonghe BC
[Ad] Endereço:Pennsylvania State University, School of Medicine, Hershey, PA, USA. Electronic address: sturgeon.katie@gmail.com.
[Ti] Título:Physical activity induced protection against breast cancer risk associated with delayed parity.
[So] Source:Physiol Behav;169:52-58, 2017 Feb 01.
[Is] ISSN:1873-507X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epidemiological evidence indicates that physical activity between menarche and first pregnancy is associated with a lower risk of breast cancer among women with at least 20years between these reproductive events. The mechanism by which physical activity during this interval confers protection is unknown. This study used a novel animal model to assess potentially protective effects of physical activity on tumor development in delayed parity. Thirty-six female Sprague Dawley rats received an i.p. injection of 50mg/kg N-methyl-N-nitrosourea (MNU) at 5weeks of age. Estrogen and progesterone pellets were implanted subcutaneously 1week (early parity, EP, n=8) or 4weeks (delayed parity, DP, n=11) following MNU injection. An additional group of DP rats were progressively exercise trained (Ex+DP, n=9) on a treadmill following MNU injection for 7weeks (up to 20m/min at 15% incline for 30min). We observed the greatest tumor latency and smallest tumor burden in Ex+DP animals. Ductal hyperplasia and inflammation of non-tumor bearing mammary glands were only found in DP, and we detected a significant increase in collagen for DP and Ex+DP compared to EP. Exercise induced differential gene expression of cyclin-dependent kinase-inhibitor 1C (Cdkn1c) and urokinase-plasminogen activator (Plau) in mammary tissue of Ex+DP animals compared to DP alone. While there are delayed parity-induced changes in mammary gland collagen and gene expression levels, Ex+DP animals had longer tumor latency, smaller tumor burden, and glandular tissue resistant to ductal hyperplasia. Exercise may induce protection through beneficial regulation of gene expression profiles.
[Mh] Termos MeSH primário: Neoplasias da Mama/prevenção & controle
Neoplasias da Mama/fisiopatologia
Paridade/fisiologia
Condicionamento Físico Animal/métodos
Prenhez/fisiologia
[Mh] Termos MeSH secundário: Alquilantes/toxicidade
Animais
Neoplasias da Mama/induzido quimicamente
Colágeno Tipo V/genética
Colágeno Tipo V/metabolismo
Inibidor de Quinase Dependente de Ciclina p57/genética
Inibidor de Quinase Dependente de Ciclina p57/metabolismo
Modelos Animais de Doenças
Feminino
Expressão Gênica/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/fisiologia
Metilnitrosoureia/toxicidade
Paridade/efeitos dos fármacos
Gravidez
Prenhez/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Tempo de Reação/fisiologia
Fatores de Tempo
Ativador de Plasminogênio Tipo Uroquinase/genética
Ativador de Plasminogênio Tipo Uroquinase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alkylating Agents); 0 (Collagen Type V); 0 (Cyclin-Dependent Kinase Inhibitor p57); 684-93-5 (Methylnitrosourea); EC 3.4.21.73 (Urokinase-Type Plasminogen Activator)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170628
[Lr] Data última revisão:
170628
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161126
[St] Status:MEDLINE


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[PMID]:27628582
[Au] Autor:Kotzé-Hörstmann LM; Keswell D; Adams K; Dlamini T; Goedecke JH
[Ad] Endereço:Division of Exercise Science and Sports Medicine, Department of Human Biology, University of Cape Town, Cape Town, South Africa.
[Ti] Título:Hypoxia and extra-cellular matrix gene expression in adipose tissue associates with reduced insulin sensitivity in black South African women.
[So] Source:Endocrine;55(1):144-152, 2017 Jan.
[Is] ISSN:1559-0100
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Black South African women are more insulin resistant and have increased gluteal subcutaneous adipose tissue hypertrophy than white South African women. We tested the hypothesis that adipose tissue hypoxia and extracellular matrix gene expression in gluteal and abdominal subcutaneous adipose tissue is higher in black than white women, and associates with reduced insulin sensitivity in black women. Insulin sensitivity (frequently sampled intravenous glucose tolerance test), gluteal and abdominal subcutaneous adipose tissue mRNA levels of hypoxia- and extracellular matrix-related genes were measured in normal-weight and obese premenopausal black (n = 30) and white (n = 26) South African women at baseline, and in black women, at 5-year follow-up (n = 10). Compared to obese white women, obese black women had higher expression of hypoxia inducible factor 1, collagen Vα1 and collagen VIα1 and reduced vascular endothelial growth factor-α expression in gluteal (p < 0.05) but not abdominal subcutaneous adipose tissue depots. Independent of age and body fatness, gluteal expression of hypoxia inducible factor 1 (r = -0.55; p = 0.01), collagen Vα1 (r = -0.41; p = 0.05) and collagen VIα1 (r = -0.47; p = 0.03) correlated with reduced insulin sensitivity in black women only. Over a 5-year follow-up, changes in gluteal hypoxia inducible factor 1 (r = 0.77; p = 0.01) collagen Vα1 (r = 0.71; p = 0.02) and collagen VIα1 (r = 0.81; p < 0.01) expression correlated positively with the change in fasting insulin concentrations in black women. Compared to their white counterparts, black women expressed higher levels of genes associated with hypoxia and collagen deposition, and the associations between these genes and insulin sensitivity differed by ethnicity. We thus propose that insulin resistance in black women may be related to higher extracellular matrix and hypoxia gene expression.
[Mh] Termos MeSH primário: Colágeno Tipo VI/metabolismo
Colágeno Tipo V/metabolismo
Fator 1 Induzível por Hipóxia/metabolismo
Resistência à Insulina
Obesidade/metabolismo
Gordura Subcutânea/metabolismo
Regulação para Cima
[Mh] Termos MeSH secundário: Adulto
Grupo com Ancestrais do Continente Africano
Índice de Massa Corporal
Estudos de Coortes
Colágeno Tipo V/genética
Colágeno Tipo VI/genética
Regulação para Baixo
Grupo com Ancestrais do Continente Europeu
Feminino
Seguimentos
Seres Humanos
Fator 1 Induzível por Hipóxia/genética
Resistência à Insulina/etnologia
Obesidade/etnologia
Projetos Piloto
Gordura Subcutânea Abdominal/metabolismo
Fator A de Crescimento do Endotélio Vascular/genética
Fator A de Crescimento do Endotélio Vascular/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (COL5A1 protein, human); 0 (Col6a1 protein, human); 0 (Collagen Type V); 0 (Collagen Type VI); 0 (Hypoxia-Inducible Factor 1); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160916
[St] Status:MEDLINE
[do] DOI:10.1007/s12020-016-1089-0


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[PMID]:27541197
[Au] Autor:Brown KL; Seale KB; El Khoury LY; Posthumus M; Ribbans WJ; Raleigh SM; Collins M; September AV
[Ad] Endereço:a Division of Exercise Science and Sports Medicine, Department of Human Biology, Faculty of Health Sciences , University of Cape Town , Cape Town , South Africa.
[Ti] Título:Polymorphisms within the COL5A1 gene and regulators of the extracellular matrix modify the risk of Achilles tendon pathology in a British case-control study.
[So] Source:J Sports Sci;35(15):1475-1483, 2017 Aug.
[Is] ISSN:1466-447X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Several genetic loci have been associated with risk of Achilles tendon pathology (ATP) within South African and Australian populations. The aim of this study was, therefore, to evaluate eight previously implicated genetic variants in an independent British population. A total of 130 asymptomatic controls (CON) and 112 participants clinically diagnosed with ATP comprising 87 individuals with chronic Achilles tendinopathy (TEN) and 25 with Achilles tendon ruptures (RUP) were included. All participants were genotyped for variants within the COL5A1, MIR608, IL-1ß, IL-6 and CASP8 genes. Primary findings implicated COL5A1 and CASP8. Three inferred allele combinations constructed from COL5A1 rs12722, rs3196378 and rs71746744 were identified as risk modifiers. The T-C-D combination was associated with increased risk of ATP (P = 0.023) and RUP (P < 0.001), the C-A-I combination was associated with increased risk of ATP (P = 0.011), TEN (P = 0.011) and RUP (P = 0.011) and the C-C-D combination was associated with decreased risk of ATP (P = 0.011) and RUP (P = 0.004). The CASP8 rs3834129 DD genotype was associated with decreased risk of TEN (P = 0.020, odds ratio: 0.45, 95% confidence interval: 0.22-0.90) and the CASP8 I-G (rs3834129-rs1045485) inferred allele combination was associated with increased risk of TEN (P = 0.031). This study further highlights the importance of polymorphisms within COL5A1 and CASP8 in the aetiology of ATP.
[Mh] Termos MeSH primário: Tendão do Calcâneo/lesões
Tendão do Calcâneo/patologia
Colágeno Tipo V/genética
Matriz Extracelular/metabolismo
Polimorfismo Genético
Ruptura/genética
Tendinopatia/genética
[Mh] Termos MeSH secundário: Adulto
Alelos
Estudos de Casos e Controles
Caspase 8/genética
Feminino
Frequência do Gene
Predisposição Genética para Doença
Genótipo
Seres Humanos
Interleucina-1beta/genética
Interleucina-6/genética
Masculino
Repetições de Microssatélites
Meia-Idade
Tendinopatia/metabolismo
Ubiquitina-Proteína Ligases/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (COL5A1 protein, human); 0 (Collagen Type V); 0 (Interleukin-1beta); 0 (Interleukin-6); EC 2.3.2.27 (MYLIP protein, human); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 3.4.22.- (CASP8 protein, human); EC 3.4.22.- (Caspase 8)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170831
[Lr] Data última revisão:
170831
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160820
[St] Status:MEDLINE
[do] DOI:10.1080/02640414.2016.1221524


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[PMID]:28005290
[Au] Autor:Connizzo BK; Adams SM; Adams TH; Birk DE; Soslowsky LJ
[Ad] Endereço:McKay Orthopaedic Research Laboratory, University of Pennsylvania, 424 Stemmler Hall, 36th and Hamilton Walk, Philadelphia, Pennsylvania, 19104-6081.
[Ti] Título:Collagen V expression is crucial in regional development of the supraspinatus tendon.
[So] Source:J Orthop Res;34(12):2154-2161, 2016 Dec.
[Is] ISSN:1554-527X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Manipulations in cell culture and mouse models have demonstrated that reduction of collagen V results in altered fibril structure and matrix assembly. A tissue-dependent role for collagen V in determining mechanical function was recently established, but its role in determining regional properties has not been addressed. The objective of this study was to define the role(s) of collagen V expression in establishing the site-specific properties of the supraspinatus tendon. The insertion and midsubstance of tendons from wild type, heterozygous and tendon/ligament-specific null mice were assessed for crimp morphology, fibril morphology, cell morphology, as well as total collagen and pyridinoline cross-link (PYD) content. Fibril morphology was altered at the midsubstance of both groups with larger, but fewer, fibrils and no change in cell morphology or collagen compared to the wild type controls. In contrast, a significant disruption of fibril assembly was observed at the insertion site of the null group with the presence of structurally aberrant fibrils. Alterations were also present in cell density and PYD content. Altogether, these results demonstrate that collagen V plays a crucial role in determining region-specific differences in mouse supraspinatus tendon structure. © 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 34:2154-2161, 2016.
[Mh] Termos MeSH primário: Colágeno Tipo V/metabolismo
Manguito Rotador/metabolismo
[Mh] Termos MeSH secundário: Animais
Colágeno Tipo V/genética
Camundongos Endogâmicos C57BL
Manguito Rotador/crescimento & desenvolvimento
Manguito Rotador/ultraestrutura
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type V)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161223
[St] Status:MEDLINE
[do] DOI:10.1002/jor.23246


  9 / 331 MEDLINE  
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[PMID]:27734993
[Au] Autor:Di Giancamillo A; Andreis ME; Taini P; Veronesi MC; Di Giancamillo M; Modina SC
[Ad] Endereço:Department of Health, Animal Science and Food Safety, University of Milan. silvia.modina@unimi.it.
[Ti] Título:Cartilage canals in newborn dogs: histochemical and immunohistochemical findings.
[So] Source:Eur J Histochem;60(3):2701, 2016 Sep 15.
[Is] ISSN:2038-8306
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Cartilage canals (CCs) are microscopic structures involved in secondary ossification centers (SOCs) development. The features of CCs were investigated in the humeral and femoral proximal epiphyses of small-sized newborn dogs (from premature to 28 days after birth) with histochemical and immunohistochemical approaches. Masson's Trichrome revealed a ring-shaped area around CCs, which changes in colour from green (immature collagen) to red (mature collagen) as ossification progresses; perichondrium staining always matched the ring colour. Safranin-O was always negative. Immunohistochemical analysis revealed immunopositivity for both collagen type I and V around the CCs; collagen type II was negative. CCs count showed a tendency to be higher in the humerus than in the femur. This work enlightened for the first time changes in composition of CCs surrounding matrix during SOCs development in dogs, paving the way to further investigations.
[Mh] Termos MeSH primário: Colágeno Tipo I/biossíntese
Colágeno Tipo V/biossíntese
Fêmur/citologia
Fêmur/metabolismo
Lâmina de Crescimento/citologia
Lâmina de Crescimento/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Cães
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type I); 0 (Collagen Type V)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161014
[St] Status:MEDLINE
[do] DOI:10.4081/ejh.2016.2701


  10 / 331 MEDLINE  
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[PMID]:27599582
[Au] Autor:Liu G; Wu K; Sheng Y
[Ad] Endereço:Department of Breast Surgery, Changhai Hospital, Second Military Medical University, Shanghai 200433, P.R. China.
[Ti] Título:Elucidation of the molecular mechanisms of anaplastic thyroid carcinoma by integrated miRNA and mRNA analysis.
[So] Source:Oncol Rep;36(5):3005-3013, 2016 Nov.
[Is] ISSN:1791-2431
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:To elucidate the complex molecular mechanisms of anaplastic thyroid carcinoma (ATC), the mRNA and miRNA expression profiles of ATC were systematically explored. A total of 55 common differentially expressed genes (DEGs) were obtained from two mRNA expression datasets including 23 ATC samples and 24 paired normal samples. Gene expression levels of three randomly selected DEGs, VCAN, COL5A1 and KCNJ16, were examined using RT-PCR in 10 ATC samples. Notably, the ATC and normal samples were clearly classified into two groups based on their common DEGs. Moreover 23 common DEGs, such as TG, NKX2-1, KCNJ16 and CTHRC1, were predicted to be the potential targets of 17 identified miRNAs in ATC. Meanwhile, several miRNA target genes were associated with biological processes related to tumor progression such as angiogenesis, cell migration or growth and potassium channel regulation. In summary, the poor prognosis of ATC is possibly caused via complex biological processes. Firstly, angiogenesis was activated by the high expression of CTHRC1, VCAN and POSTN, providing necessary nutrition for tumor cells. Then tumor distant metastasis was induced via stimulation of cell migration and cell growth or regulation of cell-cell interaction. Moreover, intracellular potassium concentration changes promoted ATC progression indirectly. Hence, identification of these critical DEGs was valuable in understanding the molecular mechanisms of ATC.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/biossíntese
Colágeno Tipo V/biossíntese
Proteínas da Matriz Extracelular/biossíntese
Canais de Potássio Corretores do Fluxo de Internalização/biossíntese
Carcinoma Anaplásico da Tireoide/genética
Versicanas/biossíntese
[Mh] Termos MeSH secundário: Moléculas de Adesão Celular/genética
Comunicação Celular
Movimento Celular/genética
Proliferação Celular/genética
Colágeno Tipo V/genética
Proteínas da Matriz Extracelular/genética
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Masculino
MicroRNAs/biossíntese
MicroRNAs/genética
Neovascularização Patológica/genética
Proteínas Nucleares/biossíntese
Proteínas Nucleares/genética
Canais de Potássio Corretores do Fluxo de Internalização/genética
Prognóstico
Carcinoma Anaplásico da Tireoide/patologia
Fator Nuclear 1 de Tireoide
Fatores de Transcrição/biossíntese
Fatores de Transcrição/genética
Versicanas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (COL5A1 protein, human); 0 (CTHRC1 protein, human); 0 (Cell Adhesion Molecules); 0 (Collagen Type V); 0 (Extracellular Matrix Proteins); 0 (Kir5.1 protein, human); 0 (MicroRNAs); 0 (Nuclear Proteins); 0 (POSTN protein, human); 0 (Potassium Channels, Inwardly Rectifying); 0 (Thyroid Nuclear Factor 1); 0 (Transcription Factors); 0 (VCAN protein, human); 126968-45-4 (Versicans)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160908
[St] Status:MEDLINE
[do] DOI:10.3892/or.2016.5064



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