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[PMID]:29223062
[Au] Autor:Kotnik P; Krajnc MK; Pahor A; Finsgar M; Knez Z
[Ad] Endereço:Department of Chemistry, Faculty of Medicine, University of Maribor, Taborska 8, SI-2000 Maribor, Slovenia; Laboratory for Separation Processes and Product Design, Faculty of Chemistry and Chemical Engineering, University of Maribor, Smetanova 17, SI-2000 Maribor, Slovenia.
[Ti] Título:HPLC-MS/MS method optimisation for matrix metalloproteinase 3 and matrix metalloproteinase 9 determination in human blood serum using target analysis.
[So] Source:J Pharm Biomed Anal;150:137-143, 2018 Feb 20.
[Is] ISSN:1873-264X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A quantitative analysis of zinc endopeptidases matrix metalloproteinase 9 (MMP9) and matrix metalloproteinase 3 (MMP3) from human blood serum are presented. Both matrix metalloproteinases (MMP) are present in human blood serum and can be used as biomarkers for different diseases. The analysis was performed using LC-MS/MS with a triple quadrupole mass spectrometer, based on two specific peptides of each MMP in comparison with an enzyme-linked immunosorbent assay (ELISA). While the conditions for the LC-MS/MS analysis of MMP9 peptides were previously reported for bronchoalveolar lavage fluid, the analysis of MMP3 peptides was newly quantified for human blood serum herein for the first time. For MMP3, the linear behaviour was determined in the concentration range from 1.0-200.0ng/mL (R =0.997) with an LLOD of 0.5ng/mL. For MMP9, linearity was determined in the concentration range from 6.5-65.0ng/mL (R =0.995) with an LLOD of 2.0ng/mL.
[Mh] Termos MeSH primário: Cromatografia Líquida de Alta Pressão/métodos
Metaloproteinase 3 da Matriz/sangue
Metaloproteinase 9 da Matriz/sangue
Espectrometria de Massas em Tandem/métodos
[Mh] Termos MeSH secundário: Ensaio de Imunoadsorção Enzimática
Seres Humanos
Limite de Detecção
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.4.24.17 (MMP3 protein, human); EC 3.4.24.17 (Matrix Metalloproteinase 3); EC 3.4.24.35 (MMP9 protein, human); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180130
[Lr] Data última revisão:
180130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171210
[St] Status:MEDLINE


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[PMID]:28973340
[Au] Autor:Wu Y; Bu J; Yang Y; Lin X; Cai X; Huang C; Zheng X; Ouyang W; Li W; Zhang X; Liu Z
[Ad] Endereço:Eye Institute of Xiamen University and Fujian Provincial Key Laboratory of Ophthalmology and Visual Science, Xiamen, Fujian, China.
[Ti] Título:Therapeutic Effect of MK2 Inhibitor on Experimental Murine Dry Eye.
[So] Source:Invest Ophthalmol Vis Sci;58(11):4898-4907, 2017 Sep 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: To investigate the role of mitogen-activated protein kinase-activated protein kinase-2 (MK2) in ocular surface damage of dry eye. Methods: MK2 inhibition was performed in mice subjected to desiccating stress (DS) by topical application of MK2 inhibitor (MK2i) or vehicle eye drops. The total and phosphorylated MK2 in conjunctiva were detected by Western blot. The phenol red cotton test was used to measure tear production, and Oregon green dextran staining was performed to assess corneal epithelial barrier function. PAS staining was used to quantify conjunctival goblet cells. Immunofluorescent staining and quantitative RT-PCR were used to assess the expression of matrix metalloproteinase (MMP)-3 and -9 in corneal epithelium. Apoptosis in ocular surface was assessed by TUNEL and immunofluorescent staining for activated caspase-3 and -8. Inflammation was evaluated by CD4+ T-cell infiltration and production of T helper (Th) cytokines, including IFN-γ, IL-13, and IL-17A in conjunctiva. Results: DS promoted MK2 activation in conjunctiva. Compared with vehicle control mice, MK2i-treated mice showed increased tear production, decreased goblet cell loss, and improved corneal barrier function. Topical MK2 inhibition decreased the expression of MMP-3 and -9 in corneal epithelium, and suppressed cell apoptosis in ocular surface under DS. Topical MK2 inhibition decreased CD4+ T-cell infiltration, with decreased production of IFN-γ and IL-17A and increased production of IL-13 in conjunctiva. Conclusions: Topical MK2 inhibition effectively alleviated ocular surface damage via suppressing cell apoptosis and CD4+ T-cell-mediated inflammation in ocular surface of dry eye.
[Mh] Termos MeSH primário: Túnica Conjuntiva/efeitos dos fármacos
Síndromes do Olho Seco/tratamento farmacológico
Peptídeos e Proteínas de Sinalização Intracelular/antagonistas & inibidores
Peptídeos e Proteínas de Sinalização Intracelular/fisiologia
Peptídeos/farmacologia
Proteínas Serina-Treonina Quinases/antagonistas & inibidores
Proteínas Serina-Treonina Quinases/fisiologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Western Blotting
Túnica Conjuntiva/metabolismo
Citocinas/metabolismo
Modelos Animais de Doenças
Síndromes do Olho Seco/metabolismo
Epitélio Anterior/efeitos dos fármacos
Epitélio Anterior/metabolismo
Células Caliciformes/metabolismo
Metaloproteinase 3 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Camundongos
Lágrimas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Intracellular Signaling Peptides and Proteins); 0 (MK2i peptide); 0 (Peptides); EC 2.7.1.- (MAP-kinase-activated kinase 2); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 3.4.24.17 (Matrix Metalloproteinase 3); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-22240


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[PMID]:28961241
[Au] Autor:Padala C; Tupurani MA; Puranam K; Gantala S; Shyamala N; Kondapalli MS; Gundapaneni KK; Mudigonda S; Galimudi RK; Kupsal K; Nanchari SR; Chavan U; Chinta SK; Mukta S; Satti V; Hanumanth SR
[Ad] Endereço:Department of Genetics, Osmania University, Hyderabad, Telangana State, India.
[Ti] Título:Synergistic effect of collagenase-1 (MMP1), stromelysin-1 (MMP3) and gelatinase-B (MMP9) gene polymorphisms in breast cancer.
[So] Source:PLoS One;12(9):e0184448, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Extracellular matrix degradation by matrix metalloproteinases (MMPs) is an important mechanism involved in tumor invasion and metastasis. Genetic variations of MMPs have shown association with multiple cancers. The present study is focused to elucidate the association of MMP-1, 3 and 9 genetic variants with respect to epidemiological and clinicopathological variables by haplotype, LD, MDR, survival in silico analyses among South Indian women. MATERIAL AND METHODS: MMP3-1171 5A/6A and MMP9-1562 C/T SNPs were genotyped by Allele specific polymerase chain reaction and MMP1-1607 1G/2G polymorphism by restriction fragment length polymorphism assays respectively, in 300 BC patients and age-matched 300 healthy controls. Statistical analysis was performed using the SNPStats and SPSS software. Linkage disequilibrium and gene-gene interactions were performed using Haploview and MDR software respectively. Further, transcription factor binding sites in the promoter regions of SNPs under study were carried out using AliBaba2.1 software. RESULTS: We have observed an increased frequency of 2G-allele of MMP1, 6A-allele of MMP3 and T-allele of MMP9 (p<0.05) respectively in BC subjects. The 2G-6A haplotype (minor alleles of MMP-1 and MMP-3 respectively) has shown an increased susceptibility to BC. Further, MMP polymorphisms were associated with the clinical characteristics of BC patients such as steroid hormone receptor status, lymph node involvement and metastasis. SNP combinations were in perfect LD in controls. MDR analysis revealed a positive interaction between the SNPs. 5-years survival rate and cox-regression analysis showed a significant association with clinicopathological variables. CONCLUSION: Our results suggest that MMP1-1607 1G/2G, MMP3-1171 5A/6A and MMP9-1562 C/T gene polymorphisms have synergistic effect on breast cancer. The interactions of MMPs clinical risk factors such as lymph node involvement has shown a strong correlation and might influence the 5-years survival rate, suggesting their potential role in the breast carcinogenesis.
[Mh] Termos MeSH primário: Neoplasias da Mama/enzimologia
Metaloproteinase 1 da Matriz/genética
Metaloproteinase 3 da Matriz/genética
Metaloproteinase 9 da Matriz/genética
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Adulto
Alelos
Neoplasias da Mama/patologia
Estudos de Casos e Controles
Feminino
Frequência do Gene
Genótipo
Haplótipos
Seres Humanos
Desequilíbrio de Ligação
Meia-Idade
Reação em Cadeia da Polimerase
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.4.24.17 (MMP3 protein, human); EC 3.4.24.17 (Matrix Metalloproteinase 3); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 3.4.24.7 (Matrix Metalloproteinase 1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170930
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184448


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[PMID]:28859141
[Au] Autor:Maccarana M; Svensson RB; Knutsson A; Giannopoulos A; Pelkonen M; Weis M; Eyre D; Warman M; Kalamajski S
[Ad] Endereço:Department of Experimental Medical Sciences, Lund University, Lund, Sweden.
[Ti] Título:Asporin-deficient mice have tougher skin and altered skin glycosaminoglycan content and structure.
[So] Source:PLoS One;12(8):e0184028, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The main structural component of connective tissues is fibrillar, cross-linked collagen whose fibrillogenesis can be modulated by Small Leucine-Rich Proteins/Proteoglycans (SLRPs). Not all SLRPs' effects on collagen and extracellular matrix in vivo have been elucidated; one of the less investigated SLRPs is asporin. Here we describe the successful generation of an Aspn-/- mouse model and the investigation of the Aspn-/- skin phenotype. Functionally, Aspn-/- mice had an increased skin mechanical toughness, although there were no structural changes present on histology or immunohistochemistry. Electron microscopy analyses showed 7% thinner collagen fibrils in Aspn-/- mice (not statistically significant). Several matrix genes were upregulated, including collagens (Col1a1, Col1a2, Col3a1), matrix metalloproteinases (Mmp2, Mmp3) and lysyl oxidases (Lox, Loxl2), while lysyl hydroxylase (Plod2) was downregulated. Intriguingly no differences were observed in collagen protein content or in collagen cross-linking-related lysine oxidation or hydroxylation. The glycosaminoglycan content and structure in Aspn-/- skin was profoundly altered: chondroitin/dermatan sulfate was more than doubled and had an altered composition, while heparan sulfate was halved and had a decreased sulfation. Also, decorin and biglycan were doubled in Aspn-/- skin. Overall, asporin deficiency changes skin glycosaminoglycan composition, and decorin and biglycan content, which may explain the changes in skin mechanical properties.
[Mh] Termos MeSH primário: Biglicano/genética
Decorina/genética
Proteínas da Matriz Extracelular/deficiência
Efeito Fundador
Regulação da Expressão Gênica
Pele/metabolismo
[Mh] Termos MeSH secundário: Aminoácido Oxirredutases/genética
Aminoácido Oxirredutases/metabolismo
Animais
Biglicano/metabolismo
Sulfatos de Condroitina/genética
Sulfatos de Condroitina/metabolismo
Colágeno Tipo I/genética
Colágeno Tipo I/metabolismo
Colágeno Tipo III/genética
Colágeno Tipo III/metabolismo
Decorina/metabolismo
Dermatan Sulfato/análogos & derivados
Dermatan Sulfato/genética
Dermatan Sulfato/metabolismo
Matriz Extracelular/genética
Matriz Extracelular/metabolismo
Proteínas da Matriz Extracelular/genética
Feminino
Heparitina Sulfato/genética
Heparitina Sulfato/metabolismo
Sulfato de Ceratano/genética
Sulfato de Ceratano/metabolismo
Masculino
Metaloproteinase 2 da Matriz/genética
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 3 da Matriz/genética
Metaloproteinase 3 da Matriz/metabolismo
Camundongos
Camundongos Knockout
Fenótipo
Pró-Colágeno-Lisina 2-Oxoglutarato 5-Dioxigenase/genética
Pró-Colágeno-Lisina 2-Oxoglutarato 5-Dioxigenase/metabolismo
Pele/ultraestrutura
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aspn protein, mouse); 0 (Biglycan); 0 (COL3A1 protein, mouse); 0 (Col1a2 protein, mouse); 0 (Collagen Type I); 0 (Collagen Type III); 0 (Dcn protein, mouse); 0 (Decorin); 0 (Extracellular Matrix Proteins); 0 (collagen type I, alpha 1 chain); 0 (dermatan sulfate chondroitin sulfate); 24967-94-0 (Dermatan Sulfate); 9007-28-7 (Chondroitin Sulfates); 9050-30-0 (Heparitin Sulfate); 9056-36-4 (Keratan Sulfate); EC 1.14.11.4 (Procollagen-Lysine, 2-Oxoglutarate 5-Dioxygenase); EC 1.14.11.4 (lysyl hydroxylase 2, mouse); EC 1.4.- (Amino Acid Oxidoreductases); EC 1.4.3.- (Loxl2 protein, mouse); EC 3.4.24.17 (Matrix Metalloproteinase 3); EC 3.4.24.17 (Mmp3 protein, mouse); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.24 (Mmp2 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184028


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[PMID]:28847716
[Au] Autor:Jia C; Zhang F; Zhu Y; Qi X; Wang Y
[Ad] Endereço:Shandong Provincial Key Lab of Ophthalmology, Shandong Eye Institute, Shandong Academy of Medical Sciences, Qingdao, China.
[Ti] Título:Public data mining plus domestic experimental study defined involvement of the old-yet-uncharacterized gene matrix-remodeling associated 7 (MXRA7) in physiopathology of the eye.
[So] Source:Gene;632:43-49, 2017 Oct 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Matrix-remodeling associated 7 (MXRA7) gene was first reported in 2002 and named so for its co-expression with several genes known to relate with matrix-remodeling. However, not any studies had been intentionally performed to characterize this gene. We started defining the functions of MXRA7 by integrating bioinformatics analysis and experimental study. Data mining of MXRA7 expression in BioGPS, Gene Expression Omnibus and EurExpress platforms highlighted high level expression of Mxra7 in murine ocular tissues. Real-time PCR was employed to measure Mxra7 mRNA in tissues of adult C57BL/6 mice and demonstrated that Mxra7 was preferentially expressed at higher level in retina, corneas and lens than in other tissues. Then the inflammatory corneal neovascularization (CorNV) model and fungal corneal infections were induced in Balb/c mice, and mRNA levels of Mxra7 as well as several matrix-remodeling related genes (Mmp3, Mmp13, Ecm1, Timp1) were monitored with RT-PCR. The results demonstrated a time-dependent Mxra7 under-expression pattern (U-shape curve along timeline), while all other matrix-remodeling related genes manifested an opposite changes pattern (dome-shape curve). When limited data from BioGPS concerning human MXRA7 gene expression in human tissues were looked at, it was found that ocular tissue was also the one expressing highest level of MXRA7. To conclude, integrative assay of MXRA7 gene expression in public databank as well as domestic animal models revealed a selective high expression MXRA7 in murine and human ocular tissues, and its change patterns in two corneal disease models implied that MXRA7 might play a role in pathological processes or diseases involving injury, neovascularization and would healing.
[Mh] Termos MeSH primário: Córnea/metabolismo
Doenças da Córnea/metabolismo
Infecções Oculares/metabolismo
Neovascularização Patológica/metabolismo
Proteínas/metabolismo
[Mh] Termos MeSH secundário: Animais
Córnea/irrigação sanguínea
Proteínas da Matriz Extracelular/genética
Proteínas da Matriz Extracelular/metabolismo
Seres Humanos
Metaloproteinase 13 da Matriz/genética
Metaloproteinase 13 da Matriz/metabolismo
Metaloproteinase 3 da Matriz/genética
Metaloproteinase 3 da Matriz/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Proteínas/genética
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Inibidor Tecidual de Metaloproteinase-1/genética
Inibidor Tecidual de Metaloproteinase-1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Ecm1 protein, mouse); 0 (Extracellular Matrix Proteins); 0 (Mxra7 protein, mouse); 0 (Proteins); 0 (RNA, Messenger); 0 (Timp1 protein, mouse); 0 (Tissue Inhibitor of Metalloproteinase-1); EC 3.4.24.- (Matrix Metalloproteinase 13); EC 3.4.24.- (Mmp13 protein, mouse); EC 3.4.24.17 (Matrix Metalloproteinase 3); EC 3.4.24.17 (Mmp3 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170830
[St] Status:MEDLINE


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[PMID]:28826677
[Au] Autor:Caria CREP; Gotardo ÉMF; Santos PS; Acedo SC; de Morais TR; Ribeiro ML; Gambero A
[Ad] Endereço:Clinical Pharmacology and Gastroenterology Unit, São Francisco University Medical School, Bragança Paulista, SP 12916-900, Brazil. Electronic address: cintiarabello@yahoo.com.br.
[Ti] Título:Extracellular matrix remodeling and matrix metalloproteinase inhibition in visceral adipose during weight cycling in mice.
[So] Source:Exp Cell Res;359(2):431-440, 2017 Oct 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Extracellular matrix (ECM) remodeling is necessary for a health adipose tissue (AT) expansion and also has a role during weight loss. We investigate the ECM alteration during weight cycling (WC) in mice and the role of matrix metalloproteinases (MMPs) was assessed using GM6001, an MMP inhibitor, during weight loss (WL). Obesity was induced in mice by a high-fat diet. Obese mice were subject to caloric restriction for WL followed by reintroduction to high-fat diet for weight regain (WR), resulting in a WC protocol. In addition, mice were treated with GM6001 during WL period and the effects were observed after WR. Activity and expression of MMPs was intense during WL. MMP inhibition during WL results in inflammation and collagen content reduction. MMP inhibition during WL period interferes with the period of subsequent expansion of AT resulting in improvements in local inflammation and systemic metabolic alterations induced by obesity. Our results suggest that MMPs inhibition could be an interesting target to improve adipose tissue inflammation during WL and to support weight cyclers.
[Mh] Termos MeSH primário: Dipeptídeos/farmacologia
Matriz Extracelular/metabolismo
Gordura Intra-Abdominal/metabolismo
Inibidores de Metaloproteinases de Matriz/farmacologia
Obesidade/enzimologia
[Mh] Termos MeSH secundário: Animais
Restrição Calórica
Colágeno/genética
Colágeno/metabolismo
Dieta Hiperlipídica/efeitos adversos
Metabolismo Energético
Matriz Extracelular/efeitos dos fármacos
Expressão Gênica
Inflamação/prevenção & controle
Gordura Intra-Abdominal/efeitos dos fármacos
Metabolismo dos Lipídeos/efeitos dos fármacos
Masculino
Metaloproteinase 12 da Matriz/genética
Metaloproteinase 12 da Matriz/metabolismo
Metaloproteinase 2 da Matriz/genética
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 3 da Matriz/genética
Metaloproteinase 3 da Matriz/metabolismo
Metaloproteinase 8 da Matriz/genética
Metaloproteinase 8 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/genética
Metaloproteinase 9 da Matriz/metabolismo
Camundongos
Obesidade/etiologia
Obesidade/genética
Obesidade/patologia
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
Ganho de Peso/efeitos dos fármacos
Perda de Peso/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dipeptides); 0 (Matrix Metalloproteinase Inhibitors); 0 (N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide); 0 (Protein Isoforms); 9007-34-5 (Collagen); EC 3.4.24.17 (Matrix Metalloproteinase 3); EC 3.4.24.17 (Mmp3 protein, mouse); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.24 (Mmp2 protein, mouse); EC 3.4.24.34 (MMP8 protein, mouse); EC 3.4.24.34 (Matrix Metalloproteinase 8); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 3.4.24.35 (Mmp9 protein, mouse); EC 3.4.24.65 (Matrix Metalloproteinase 12); EC 3.4.24.65 (matrix metallopeptidase 12, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE


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[PMID]:28718374
[Au] Autor:Sun Y; Fan X; Zhang Q; Shi X; Xu G; Zou C
[Ad] Endereço:1 Department of Laboratory, Laiwu Maternal and Child Health Care Hospital, Laiwu, China.
[Ti] Título:Cancer-associated fibroblasts secrete FGF-1 to promote ovarian proliferation, migration, and invasion through the activation of FGF-1/FGFR4 signaling.
[So] Source:Tumour Biol;39(7):1010428317712592, 2017 Jul.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ovarian cancer is the most lethal gynecologic malignancy, due to its high propensity for metastasis. Cancer-associated fibroblasts, as the dominant component of tumor microenvironment, are crucial for tumor progression. However, the mechanisms underlying the regulation of ovarian cancer cells by cancer-associated fibroblasts remain little known. Here, we first isolated cancer-associated fibroblasts from patients' ovarian tissues and found that cancer-associated fibroblasts promoted SKOV3 cells' proliferation, migration, and invasion. Fibroblast growth factor-1 was identified as a highly increased factor in cancer-associated fibroblasts compared with normal fibroblasts by quantitative reverse transcription polymerase chain reaction (~4.6-fold, p < 0.01) and ELISA assays (~4-fold, p < 0.01). High expression of fibroblast growth factor-1 in cancer-associated fibroblasts either naturally or through gene recombination led to phosphorylation of fibroblast growth factor receptor 4 in SKOV3 cells, which is followed by the activation of mitogen-activated protein kinase/extracellular signal-regulated protein kinase pathway and epithelial-to-mesenchymal transition-associated gene Snail1 and MMP3 expression. Moreover, treatment of SKOV3 cell with fibroblast growth factor receptor inhibitor PD173074 terminated cellular proliferation, migration, and invasion, reduced the phosphorylation level of fibroblast growth factor receptor 4, and suppressed the activation of mitogen-activated protein kinase/extracellular signal-regulated protein kinase pathway. In addition, the expression level of Snail1 and MMP3 was reduced, while the expression level of E-cadherin increased. These observations suggest a crucial role for cancer-associated fibroblasts and fibroblast growth factor-1/fibroblast growth factor receptor 4 signaling in the progression of ovarian cancer. Therefore, this fibroblast growth factor-1/fibroblast growth factor receptor 4 axis may become a potential target for the treatment of ovarian cancer.
[Mh] Termos MeSH primário: Fator 1 de Crescimento de Fibroblastos/genética
Metaloproteinase 3 da Matriz/genética
Neoplasias Ovarianas/genética
Receptor Tipo 4 de Fator de Crescimento de Fibroblastos/genética
Fatores de Transcrição da Família Snail/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Animais
Caderinas/genética
Fibroblastos Associados a Câncer/metabolismo
Fibroblastos Associados a Câncer/patologia
Linhagem Celular Tumoral
Movimento Celular/genética
Proliferação Celular/genética
Feminino
Fator 1 de Crescimento de Fibroblastos/biossíntese
Regulação Neoplásica da Expressão Gênica/genética
Seres Humanos
Metaloproteinase 3 da Matriz/biossíntese
Meia-Idade
Invasividade Neoplásica/genética
Neoplasias Ovarianas/patologia
Receptor Tipo 4 de Fator de Crescimento de Fibroblastos/biossíntese
Transdução de Sinais
Fatores de Transcrição da Família Snail/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cadherins); 0 (SNAI1 protein, human); 0 (Snail Family Transcription Factors); 104781-85-3 (Fibroblast Growth Factor 1); EC 2.7.10.1 (FGFR4 protein, human); EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 4); EC 3.4.24.17 (MMP3 protein, human); EC 3.4.24.17 (Matrix Metalloproteinase 3)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317712592


  8 / 3717 MEDLINE  
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[PMID]:28708839
[Au] Autor:Loupasakis K; Kuo D; Sokhi UK; Sohn C; Syracuse B; Giannopoulou EG; Park SH; Kang H; Rätsch G; Ivashkiv LB; Kalliolias GD
[Ad] Endereço:Arthritis and Tissue Degeneration Program and David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, United States of America.
[Ti] Título:Tumor Necrosis Factor dynamically regulates the mRNA stabilome in rheumatoid arthritis fibroblast-like synoviocytes.
[So] Source:PLoS One;12(7):e0179762, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During rheumatoid arthritis (RA), Tumor Necrosis Factor (TNF) activates fibroblast-like synoviocytes (FLS) inducing in a temporal order a constellation of genes, which perpetuate synovial inflammation. Although the molecular mechanisms regulating TNF-induced transcription are well characterized, little is known about the impact of mRNA stability on gene expression and the impact of TNF on decay rates of mRNA transcripts in FLS. To address these issues we performed RNA sequencing and genome-wide analysis of the mRNA stabilome in RA FLS. We found that TNF induces a biphasic gene expression program: initially, the inducible transcriptome consists primarily of unstable transcripts but progressively switches and becomes dominated by very stable transcripts. This temporal switch is due to: a) TNF-induced prolonged stabilization of previously unstable transcripts that enables progressive transcript accumulation over days and b) sustained expression and late induction of very stable transcripts. TNF-induced mRNA stabilization in RA FLS occurs during the late phase of TNF response, is MAPK-dependent, and involves several genes with pathogenic potential such as IL6, CXCL1, CXCL3, CXCL8/IL8, CCL2, and PTGS2. These results provide the first insights into genome-wide regulation of mRNA stability in RA FLS and highlight the potential contribution of dynamic regulation of the mRNA stabilome by TNF to chronic synovitis.
[Mh] Termos MeSH primário: Estabilidade de RNA/efeitos dos fármacos
RNA Mensageiro/metabolismo
Fator de Necrose Tumoral alfa/farmacologia
[Mh] Termos MeSH secundário: Artrite Reumatoide/metabolismo
Artrite Reumatoide/patologia
Células Cultivadas
Quimiocinas/genética
Quimiocinas/metabolismo
Ciclo-Oxigenase 2/genética
Ciclo-Oxigenase 2/metabolismo
Citocinas/genética
Citocinas/metabolismo
Fibroblastos/citologia
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Interleucina-6/genética
Interleucina-6/metabolismo
Metaloproteinase 3 da Matriz/genética
Metaloproteinase 3 da Matriz/metabolismo
RNA/química
RNA/isolamento & purificação
RNA/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Análise de Sequência de RNA
Sinoviócitos/citologia
Sinoviócitos/efeitos dos fármacos
Sinoviócitos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokines); 0 (Cytokines); 0 (Interleukin-6); 0 (RNA, Messenger); 0 (Tumor Necrosis Factor-alpha); 63231-63-0 (RNA); EC 1.14.99.1 (Cyclooxygenase 2); EC 3.4.24.17 (Matrix Metalloproteinase 3)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170715
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179762


  9 / 3717 MEDLINE  
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[PMID]:28667931
[Au] Autor:Karpec D; Rudys R; Leonaviciene L; Mackiewicz Z; Bradunaite R; Kirdaite G; Venalis A
[Ad] Endereço:State Research Institute Centre for Innovative Medicine, Santariskiu St. 5, LT-08406 Vilnius, Lithuania; Vilnius University, Faculty of Medicine, Center of Rheumatology, Santariskiu St. 2, LT-08661 Vilnius, Lithuania. Electronic address: diana.karpec@santa.lt.
[Ti] Título:The impact of high-dose narrowband ultraviolet A1 on dermal thickness, collagen and matrix-metalloproteinases in animal model of scleroderma.
[So] Source:J Photochem Photobiol B;173:448-455, 2017 Aug.
[Is] ISSN:1873-2682
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The main purpose of the present study was to define the impact of high-dose of 365±5nm ultraviolet A1 (UVA1) on dermal fibrosis in the pre-established, bleomycin-induced mouse model of scleroderma. METHODS: DBA/2 strain mice with the pre-established, bleomycin-induced scleroderma were irradiated with cumulative UVA1 dose of 1200J/cm and in parallel were challenged with prolonged administration of bleomycin. Non-treated groups served as the control. Light source emitting a narrow band UVA1 light of 365±5nm and 21mW/cm power density was used in the study. Histological analysis was performed for the evaluation of dermal thickness. The expressions of matrix-metalloproteinase-1 (MMP-1), matrix-metalloproteinase-3 (MMP-3), collagen types I and III were evaluated by immunohistochemical analyses. The Mann - Whitney U test was used for statistical analysis. RESULTS: Dermal thickness in mice injected with bleomycin during all the experiment (8weeks) and irradiated with UVA1 for the last 5weeks was significantly lower than that in mice challenged only with bleomycin for 8weeks (253.96±31.83µm and 497.43±57.83µm, respectively; P=0.002). The dermal thickness after phototherapy was lower as compared with the pre-existing fibrotic changes observed after 3weeks of bleomycin injections (253.96±31.83µm and 443.87±41.76µm, respectively; P=0.002). High-dose of UVA1 induced the 5.8- and 5.2-fold increase in MMP-1 and MMP-3 expressions, respectively, and the 1.2- and 1.4-fold decrease in collagen type I and collagen type III expressions in the pre-established, bleomycin-induced scleroderma model as compared to that in the control non-irradiated mice (P=0.002). CONCLUSIONS: Our study has demonstrated that a cumulative 365±5nm UVA1 radiation dosage of 1200J/cm not only prevents the progression of dermal fibrosis, but also induces a regression of pre-existing fibrotic changes.
[Mh] Termos MeSH primário: Colágeno/metabolismo
Derme/efeitos da radiação
Metaloproteinases da Matriz/metabolismo
Esclerodermia Localizada/radioterapia
Raios Ultravioleta
[Mh] Termos MeSH secundário: Animais
Bleomicina/toxicidade
Colágeno Tipo I/metabolismo
Colágeno Tipo III/metabolismo
Derme/fisiologia
Modelos Animais de Doenças
Feminino
Imuno-Histoquímica
Metaloproteinase 1 da Matriz/metabolismo
Metaloproteinase 3 da Matriz/metabolismo
Camundongos
Camundongos Endogâmicos DBA
Esclerodermia Localizada/induzido quimicamente
Pregas Cutâneas
Terapia Ultravioleta
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type I); 0 (Collagen Type III); 11056-06-7 (Bleomycin); 9007-34-5 (Collagen); EC 3.4.24.- (Matrix Metalloproteinases); EC 3.4.24.17 (Matrix Metalloproteinase 3); EC 3.4.24.7 (Matrix Metalloproteinase 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170702
[St] Status:MEDLINE


  10 / 3717 MEDLINE  
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[PMID]:28657528
[Au] Autor:Ricarte-Bratti JP; Brizuela NY; Jaime-Albarran N; Montrull HL
[Ti] Título:IL-6, MMP 3 and prognosis in previously healthy sepsis patients.
[Ti] Título:IL-6, MMP-3 y pronóstico en pacientes con sepsis previamente sanos..
[So] Source:Rev Fac Cien Med Univ Nac Cordoba;74(2):99-106, 2017.
[Is] ISSN:1853-0605
[Cp] País de publicação:Argentina
[La] Idioma:eng
[Ab] Resumo:Sepsis and septic shock are clinical conditions with high mortality despite advances in technology and are the leading cause of death in intensive care. Clinical manifestations and morbidity may be attributable to a disproportionate increase in proinflammatory cytokines. The aim of this study was to evaluate the ability to predict mortality from interleukin 6 [IL-6] and matrix metalloproteinase 3 [MMP-3]. This single-center, observational, prospective study included 48 adult patients admitted to the Hospital Nacional de Clinicas in Cordoba, Argentina, with sepsis or septic shock. Serum levels of IL-6 and MMP-3 were measured at the time of diagnosis and 72 hours later. At time of admission, MMP-3 was 13.77 mg/ml in patients who died and 10.55 mg/ml in patients who survived up to 28 days after hospitalization [p = 0.012], while IL-6 did not differ between the groups. The change in IL-6 over 72 hours was increased in nonsurvivors by 21.11 ± 11.81 pg/ml and decreased in survivors by 40.87 ± 14.94 pg/ml [p = 0.007]. No difference in the change of MMP-3 over 72 hours was observed between survivors and nonsurvivors. This study shows that MMP-3 at admission and the change in IL-6 over the first 72 hours of hospitalization could provide prognostic information in septic patients. Further studies are needed to define the utility of these cytokines as a measure of sepsis severity and as predictors of mortality.
[Mh] Termos MeSH primário: Interleucina-6/sangue
Metaloproteinase 3 da Matriz/sangue
Sepse/sangue
Sepse/mortalidade
[Mh] Termos MeSH secundário: Idoso
Biomarcadores/sangue
Feminino
Seres Humanos
Masculino
Meia-Idade
Valor Preditivo dos Testes
Prognóstico
Estudos Prospectivos
Choque Séptico/sangue
Choque Séptico/mortalidade
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Biomarkers); 0 (IL6 protein, human); 0 (Interleukin-6); EC 3.4.24.17 (MMP3 protein, human); EC 3.4.24.17 (Matrix Metalloproteinase 3)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170629
[St] Status:MEDLINE



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