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[PMID]:29186710
[Au] Autor:Chen L; Tang J; Feng Y; Li S; Xiang Q; He X; Ren G; Peng W; Xiang T
[Ti] Título:ADAMTS9 is Silenced by Epigenetic Disruption in Colorectal Cancer and Inhibits Cell Growth and Metastasis by Regulating Akt/p53 Signaling.
[So] Source:Cell Physiol Biochem;44(4):1370-1380, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: ADAMTS (disintegrin-like and metalloproteinase with thrombospondin motifs) proteins are extracellular zinc metalloproteinases that play an important role in extracellular matrix assembly and degradation, connective tissue structuring, angiogenesis, and cell migration. Multiple studies suggest that ADAMTS proteins (e.g. ADAMTS9) can act as tumor suppressors. In gastric, esophageal, and nasopharyngeal carcinomas ADAMTS9 is frequently down-regulated by promoter methylation. Whether ADAMTS9 can function as a tumor suppressor gene (TSG) in colorectal cancer is still unclear. METHODS: We performed immunohistochemistry, RT-PCR, and qRT-PCR, to examine the expression of ADAMTS9 in colorectal cancer cell lines and primary colorectal cancer tissues. Methylation-specific PCR was also carried out to investigate the promoter methylation status of ADAMTS9. We also explored the functions of ADAMTS9 in colorectal cancer cell lines through in vitro experiments. RESULTS: ADAMTS9 expression was down-requlated or silenced in 83.3% (5/6) of colorectal cancer cell lines, and frequently repressed in 65.6% (21/32) of colorectal cancer tissues. Down-regulation of ADAMTS9 was partially due to promoter methylation. Exogenous expression of ADAMTS9 in colorectal cancer cell lines inhibited cell proliferation and migration through the regulation of cell cycle and apoptosis. In addition, ADAMTS9 prevented the activation of Akt, and its downstream targets in colorectal cancer cell lines. CONCLUSION: Our findings suggest ADAMTS9 is a TSG in colorectal cancer.
[Mh] Termos MeSH primário: Proteína ADAMTS9/metabolismo
Neoplasias Colorretais/patologia
Proteínas Proto-Oncogênicas c-akt/metabolismo
Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Proteína ADAMTS9/antagonistas & inibidores
Proteína ADAMTS9/genética
Apoptose
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Neoplasias Colorretais/genética
Neoplasias Colorretais/metabolismo
Ilhas de CpG
Metilação de DNA
Regulação para Baixo
Transição Epitelial-Mesenquimal
Pontos de Checagem da Fase G1 do Ciclo Celular
Vetores Genéticos/genética
Vetores Genéticos/metabolismo
Células HCT116
Seres Humanos
Imuno-Histoquímica
Regiões Promotoras Genéticas
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Transdução de Sinais
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Small Interfering); 0 (Tumor Suppressor Protein p53); 0 (Vascular Endothelial Growth Factor A); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.4.24.- (ADAMTS9 Protein); EC 3.4.24.- (ADAMTS9 protein, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1159/000485534


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[PMID]:28766346
[Au] Autor:Yaykasli KO; Hatipoglu OF; Yaykasli E; Kaya E; Ozsahin M; Uslu M
[Ti] Título:Dose-dependent effects of adiponectin on ADAMTS-9 gene expression in human chondrocytes.
[So] Source:Bratisl Lek Listy;118(7):386-390, 2017.
[Is] ISSN:0006-9248
[Cp] País de publicação:Slovakia
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS), comprising of 19 members is a family of peptidases. They have several vital functions in physiological and pathological processes in organisms. ADAMTS-9 has aggrecanolytic activity and is responsible for degradation of aggrecan mainly in articular cartilage. It is known that adiponectin is the most abundantly secreted adipokine (adipocytokines), and the characteristics of adiponectin have not been elucidated yet. It was assumed that adiponectin has anti-inflammatory effect before. However, an inflammatory feature of adiponectin was shown in researches. In our study, the effect of adiponectin on ADAMTS-9 gene expression in primary human chondrocytes was investigated. METHODS: Primary human chondrocytes were exposed to adiponectin at 1, 4, 8 and 12 µg/ml doses for certain time period. Total RNA was isolated and reverse-transcribed by random primer after incubation. ADAMTS-9 and ß-actin genes expression levels were determined using real-time polymerase chain reaction (qRT-PCR). RESULTS: The highest upregulation of ADAMTS-9 gene expression level was found at 12 µg/ml dose of adiponectin and 48 h incubation. CONCLUSION: Adiponectin is the key element in the maintenance of cartilage homeostasis. Similarly, the involvement of adiponectin in articular inflammatory diseases was demonstrated in detail. These findings bring adiponectin into central place in the research to develop adiponectin based new therapy methods for arthritic diseases. Together with these findings, our results suggest that adiponectin may be involved in the degradation of articular cartilage by increasing ADAMTS-9 gene expression (Tab. 1, Fig. 3, Ref. 35).
[Mh] Termos MeSH primário: Proteína ADAMTS9/metabolismo
Actinas/metabolismo
Adiponectina/metabolismo
Regulação Enzimológica da Expressão Gênica
[Mh] Termos MeSH secundário: Condrócitos/metabolismo
Técnicas de Transferência de Genes
Seres Humanos
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ADIPOQ protein, human); 0 (Actins); 0 (Adiponectin); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.4.24.- (ADAMTS9 Protein); EC 3.4.24.- (ADAMTS9 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170803
[St] Status:MEDLINE
[do] DOI:10.4149/BLL_2017_075


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[PMID]:28406917
[Au] Autor:Rivollier F; Chaumette B; Bendjemaa N; Chayet M; Millet B; Jaafari N; Barhdadi A; Lemieux Perreault LP; Provost S; Dubé MP; Gaillard R; Krebs MO; Kebir O
[Ad] Endereço:Université Paris Descartes, Université Paris Sorbonne Paris Cité, Centre de Psychiatrie et Neurosciences, UMR S 894, Paris, France.
[Ti] Título:Methylomic changes in individuals with psychosis, prenatally exposed to endocrine disrupting compounds: Lessons from diethylstilbestrol.
[So] Source:PLoS One;12(4):e0174783, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In the Western world, between 1940 and 1970, more than 2 million people were exposed in utero to diethylstilbestrol (DES). In exposed individuals, and in their descendants, adverse outcomes have been linked to such exposure, including cancers, genital malformations, and less consistently, psychiatric disorders. We aimed to explore whether prenatal DES exposure would be associated with DNA methylation changes, and whether these epigenetic modifications would be associated with increased risk of psychosis. METHODS: From 247 individuals born from mothers exposed to DES, we selected 69 siblings from 30 families. In each family, at least one sibling was exposed in utero to DES. We performed a methylome-wide association study using HumanMethylation450 DNA Analysis BeadChip® in peripheral blood. We analyzed methylation changes at individual CpGs or regions in exposed (n = 37) versus unexposed individuals (n = 32). We also compared exposed individuals with (n = 7) and without psychosis (n = 30). RESULTS: There were more individuals with schizophrenia in the DES-exposed group. We found no significant differences between exposed and unexposed individuals with respect to differentially methylated CpGs or regions. The largest difference was in a region near the promoter of an ADAMTS proteoglycanase gene (ADAMTS9). Compared to exposed individuals without psychosis, exposed individuals with psychosis had differential methylation in the region encompassing the gene encoding the zinc finger protein 57 (ZFP57). CONCLUSIONS: In utero exposure to DES was not associated with methylation changes at specific CpG or regions. In exposed individuals, however, psychosis was associated with specific methylomic modifications that could impact neurodevelopment and neuroplasticity.
[Mh] Termos MeSH primário: Metilação de DNA
Dietilestilbestrol/toxicidade
Epigênese Genética
Exposição Materna/efeitos adversos
Efeitos Tardios da Exposição Pré-Natal/metabolismo
Transtornos Psicóticos/metabolismo
[Mh] Termos MeSH secundário: Proteína ADAMTS9/metabolismo
Adulto
Ilhas de CpG
Proteínas de Ligação a DNA/metabolismo
Feminino
Seres Humanos
Masculino
Gravidez
Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente
Efeitos Tardios da Exposição Pré-Natal/fisiopatologia
Regiões Promotoras Genéticas
Transtornos Psicóticos/etiologia
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:CLINICAL TRIAL; COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (Transcription Factors); 0 (Zfp-57 protein, human); 731DCA35BT (Diethylstilbestrol); EC 3.4.24.- (ADAMTS9 Protein); EC 3.4.24.- (ADAMTS9 protein, human)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170504
[Lr] Data última revisão:
170504
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170414
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0174783


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[PMID]:28225792
[Au] Autor:Lin E; Tsai SJ; Kuo PH; Liu YL; Yang AC; Kao CF; Yang CH
[Ad] Endereço:Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan.
[Ti] Título:The ADAMTS9 gene is associated with cognitive aging in the elderly in a Taiwanese population.
[So] Source:PLoS One;12(2):e0172440, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Evidence indicates that the pathophysiologic mechanisms associated with insulin resistance may contribute to cognitive aging and Alzheimer's diseases. In this study, we hypothesize that single nucleotide polymorphisms (SNPs) within insulin resistance-associated genes, such as the ADAM metallopeptidase with thrombospondin type 1 motif 9 (ADAMTS9), glucokinase regulator (GCKR), and peroxisome proliferator activated receptor gamma (PPARG) genes, may be linked with cognitive aging independently and/or through complex interactions in an older Taiwanese population. A total of 547 Taiwanese subjects aged over 60 years from the Taiwan Biobank were analyzed. Mini-Mental State Examinations (MMSE) were administered to all subjects, and MMSE scores were used to measure cognitive functions. Our data showed that four SNPs (rs73832338, rs9985304, rs4317088, and rs9831846) in the ADAMTS9 gene were significantly associated with cognitive aging among the subjects (P = 1.5 x 10-6 ~ 0.0002). This association remained significant after performing Bonferroni correction. Additionally, we found that interactions between the ADAMTS9 rs9985304 and ADAMTS9 rs76346246 SNPs influenced cognitive aging (P < 0.001). However, variants in the GCKR and PPARG genes had no association with cognitive aging in our study. Our study indicates that the ADAMTS9 gene may contribute to susceptibility to cognitive aging independently as well as through SNP-SNP interactions.
[Mh] Termos MeSH primário: Proteína ADAMTS9/genética
Envelhecimento Cognitivo/fisiologia
Envelhecimento Cognitivo/psicologia
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética
Idoso
Idoso de 80 Anos ou mais
Bases de Dados Genéticas
Feminino
Estudos de Associação Genética
Genótipo
Seres Humanos
Masculino
Meia-Idade
Testes Neuropsicológicos
PPAR gama/genética
Taiwan
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (GCKR protein, human); 0 (PPAR gamma); EC 3.4.24.- (ADAMTS9 Protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170223
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0172440


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[PMID]:27982477
[Au] Autor:Gaucherand L; Falk BA; Evanko SP; Workman G; Chan CK; Wight TN
[Ad] Endereço:Matrix Biology Program, Benaroya Research Institute, Seattle, Washington.
[Ti] Título:Crosstalk Between T Lymphocytes and Lung Fibroblasts: Generation of a Hyaluronan-Enriched Extracellular Matrix Adhesive for Monocytes.
[So] Source:J Cell Biochem;118(8):2118-2130, 2017 Aug.
[Is] ISSN:1097-4644
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In immunity and inflammation, T cells are often associated with stromal mesenchymal cells such as fibroblasts. Hyaluronan and proteins that associate with hyaluronan such as versican and tumor necrosis factor-inducible gene-6 (TSG-6) are extracellular matrix (ECM) components that promote leukocyte adhesion, accumulation, and activation. However, the factors responsible for producing this specialized ECM and its impact on inflammatory events are not well understood. In this study, we explored the role of T cells in stimulating lung fibroblasts to produce an ECM that impacts monocyte adhesion. We found that CD3/CD28-activated human CD4+ T cells when co-cultured with human lung fibroblasts stimulated the expression of mRNA for hyaluronan synthase 2 (HAS2) and decreased the expression of hyaluronidase 2 (HYAL2). This led to an increase in the deposition of hyaluronan that formed cable-like structures within the ECM. Co-culturing activated T cells with fibroblasts also led to increased expression and accumulation of TSG-6. Surprisingly, addition of activated CD4+ T cells to the fibroblasts reduced the expression of mRNA for versican, and increased the expression of enzymes that degrade versican, such as ADAMTS4 and ADAMTS9 (a disintegrin and metalloproteinase with a thrombospondin type-1 motif) leading to a decrease in versican in the ECM of the co-cultures. Furthermore, addition of human monocytes to these co-cultures resulted in elevated monocyte adhesion to the cable-like structures in the ECM when compared to controls. These results illustrate the importance of crosstalk between T cells and fibroblasts in promoting the generation of a matrix that is adhesive for monocytes. J. Cell. Biochem. 118: 2118-2130, 2017. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Matriz Extracelular/imunologia
Fibroblastos/imunologia
Ácido Hialurônico/biossíntese
Monócitos/imunologia
Versicanas/biossíntese
[Mh] Termos MeSH secundário: Proteína ADAMTS4/genética
Proteína ADAMTS4/imunologia
Proteína ADAMTS9/genética
Proteína ADAMTS9/imunologia
Linfócitos T CD4-Positivos/citologia
Adesão Celular
Moléculas de Adesão Celular/genética
Moléculas de Adesão Celular/imunologia
Comunicação Celular
Técnicas de Cocultura
Matriz Extracelular/metabolismo
Fibroblastos/citologia
Proteínas Ligadas por GPI/genética
Proteínas Ligadas por GPI/imunologia
Regulação da Expressão Gênica
Glucuronosiltransferase/genética
Glucuronosiltransferase/imunologia
Seres Humanos
Hialuronan Sintases
Ácido Hialurônico/imunologia
Hialuronoglucosaminidase/genética
Hialuronoglucosaminidase/imunologia
Pulmão/citologia
Pulmão/imunologia
Ativação Linfocitária
Monócitos/citologia
Cultura Primária de Células
Transdução de Sinais
Versicanas/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (GPI-Linked Proteins); 0 (TNFAIP6 protein, human); 126968-45-4 (Versicans); 9004-61-9 (Hyaluronic Acid); EC 2.4.1.17 (Glucuronosyltransferase); EC 2.4.1.212 (HAS2 protein, human); EC 2.4.1.212 (Hyaluronan Synthases); EC 3.2.1.25 (Hyal2 protein, human); EC 3.2.1.35 (Hyaluronoglucosaminidase); EC 3.4.24.- (ADAMTS9 Protein); EC 3.4.24.- (ADAMTS9 protein, human); EC 3.4.24.82 (ADAMTS4 Protein)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161217
[St] Status:MEDLINE
[do] DOI:10.1002/jcb.25842


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[PMID]:27297885
[Au] Autor:Benz BA; Nandadasa S; Takeuchi M; Grady RC; Takeuchi H; LoPilato RK; Kakuda S; Somerville RPT; Apte SS; Haltiwanger RS; Holdener BC
[Ad] Endereço:Department of Biochemistry and Cell Biology, Stony Brook University, Stony Brook, NY, United States.
[Ti] Título:Genetic and biochemical evidence that gastrulation defects in Pofut2 mutants result from defects in ADAMTS9 secretion.
[So] Source:Dev Biol;416(1):111-122, 2016 08 01.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Protein O-fucosyltransferase 2 (POFUT2) adds O-linked fucose to Thrombospondin Type 1 Repeats (TSR) in 49 potential target proteins. Nearly half the POFUT2 targets belong to the A Disintegrin and Metalloprotease with ThromboSpondin type-1 motifs (ADAMTS) or ADAMTS-like family of proteins. Both the mouse Pofut2 RST434 gene trap allele and the Adamts9 knockout were reported to result in early embryonic lethality, suggesting that defects in Pofut2 mutant embryos could result from loss of O-fucosylation on ADAMTS9. To address this question, we compared the Pofut2 and Adamts9 knockout phenotypes and used Cre-mediated deletion of Pofut2 and Adamts9 to dissect the tissue-specific role of O-fucosylated ADAMTS9 during gastrulation. Disruption of Pofut2 using the knockout (LoxP) or gene trap (RST434) allele, as well as deletion of Adamts9, resulted in disorganized epithelia (epiblast, extraembryonic ectoderm, and visceral endoderm) and blocked mesoderm formation during gastrulation. The similarity between Pofut2 and Adamts9 mutants suggested that disruption of ADAMTS9 function could be responsible for the gastrulation defects observed in Pofut2 mutants. Consistent with this prediction, CRISPR/Cas9 knockout of POFUT2 in HEK293T cells blocked secretion of ADAMTS9. We determined that Adamts9 was dynamically expressed during mouse gastrulation by trophoblast giant cells, parietal endoderm, the most proximal visceral endoderm adjacent to the ectoplacental cone, extraembryonic mesoderm, and anterior primitive streak. Conditional deletion of either Pofut2 or Adamts9 in the epiblast rescues the gastrulation defects, and identified a new role for O-fucosylated ADAMTS9 during morphogenesis of the amnion and axial mesendoderm. Combined, these results suggested that loss of ADAMTS9 function in the extra embryonic tissue is responsible for gastrulation defects in the Pofut2 knockout. We hypothesize that loss of ADAMTS9 function in the most proximal visceral endoderm leads to slippage of the visceral endoderm and altered characteristics of the extraembryonic ectoderm. Consequently, loss of input from the extraembryonic ectoderm and/or compression of the epiblast by Reichert's membrane blocks gastrulation. In the future, the Pofut2 and Adamts9 knockouts will be valuable tools for understanding how local changes in the properties of the extracellular matrix influence the organization of tissues during mammalian development.
[Mh] Termos MeSH primário: Proteína ADAMTS9/secreção
Fucosiltransferases/genética
Gastrulação/genética
Mutação
[Mh] Termos MeSH secundário: Proteína ADAMTS9/genética
Proteína ADAMTS9/fisiologia
Âmnio/embriologia
Animais
Padronização Corporal
Linhagem Celular
Células-Tronco Embrionárias
Feminino
Células HEK293
Seres Humanos
Masculino
Mesoderma/embriologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 2.4.1.- (Fucosyltransferases); EC 2.4.1.221 (PoFut2 protein, mouse); EC 3.4.24.- (ADAMTS9 Protein); EC 3.4.24.- (Adamts9 protein, mouse)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160615
[St] Status:MEDLINE


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[PMID]:27146815
[Au] Autor:Karakose M; Demircan K; Tutal E; Demirci T; Arslan MS; Sahin M; Celik HT; Kazanci F; Karakaya J; Cakal E; Delibasi T
[Ad] Endereço:Department of Endocrinology and Metabolism, Diskapi Yildirim Beyazit Training and Research Hospital, Irfan Bastug Caddesi, 06110, Ankara, Turkey. meliakarakose@yahoo.com.
[Ti] Título:Clinical significance of ADAMTS1, ADAMTS5, ADAMTS9 aggrecanases and IL-17A, IL-23, IL-33 cytokines in polycystic ovary syndrome.
[So] Source:J Endocrinol Invest;39(11):1269-1275, 2016 Nov.
[Is] ISSN:1720-8386
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders among women of reproductive age. A disintegrin and metalloproteinase with thrombospondin-like motifs (ADAMTS) are involved in inflammation and fertility. The aim of this investigation was to evaluate the serum levels of ADAMTS1, ADAMTS5, ADAMTS9, IL-17, IL-23, IL-33 and to find out the relationship between these inflammatory cytokines and ADAMTSs in PCOS patients. METHODS: A case-control study was performed in a training and research hospital. Eighty patients with PCOS and seventy-eight healthy female volunteers were recruited in the present study. Serum ADAMTS and IL levels were determined by a human enzyme-linked immunoassay (ELISA) in all subjects. RESULTS: The IL-17A, IL-23 and IL-33 levels were significantly higher in the PCOS patients compared to the controls (p < 0.05). We could not find significant difference between the groups in terms of ADAMTS1, ADAMTS5 and ADAMTS9 levels. IL-17A had positive correlations with LDL cholesterol and IL-33 and negative correlations with ADAMTS1, ADAMTS5, and ADAMTS9. IL-33 had positive correlation with LDL cholesterol and IL-17A. In ROC curve analysis, PCOS can be predicted by the use of IL-17A, IL-23 and IL-33 which at a cut-off value of 8.37 pg/mL (44 % sensitivity, 83 % specificity), 26.75 pg/mL (36 % sensitivity, 64 % specificity) and 14.28 pg/mL (83 % sensitivity, 39 % specificity), respectively. CONCLUSIONS: The results of the study might suggest that ADAMTS and IL molecules have a role in the pathogenesis of the PCOS. Further efforts are needed to establish causality for ADAMTS-IL axis.
[Mh] Termos MeSH primário: Proteína ADAMTS1/sangue
Proteína ADAMTS5/sangue
Proteína ADAMTS9/sangue
Biomarcadores/sangue
Interleucina-17/sangue
Interleucina-23/sangue
Interleucina-33/sangue
Síndrome do Ovário Policístico/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Estudos de Casos e Controles
Citocinas/sangue
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Síndrome do Ovário Policístico/sangue
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cytokines); 0 (IL17A protein, human); 0 (IL33 protein, human); 0 (Interleukin-17); 0 (Interleukin-23); 0 (Interleukin-33); EC 3.4.24.- (ADAMTS1 Protein); EC 3.4.24.- (ADAMTS1 protein, human); EC 3.4.24.- (ADAMTS5 Protein); EC 3.4.24.- (ADAMTS5 protein, human); EC 3.4.24.- (ADAMTS9 Protein); EC 3.4.24.- (ADAMTS9 protein, human)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160506
[St] Status:MEDLINE


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[PMID]:26620591
[Au] Autor:Barreto-Luis A; Pino-Yanes M; Corrales A; Campo P; Callero A; Acosta-Herrera M; Cumplido J; Ma SF; Martinez-Tadeo J; Villar J; Garcia JG; Carrillo T; Carracedo Á; Blanca M; Flores C
[Ad] Endereço:Research Unit, Hospital Universitario N.S. de Candelaria, Tenerife, Spain; Applied Genomics Group (G2A), Genetics Laboratory, Instituto Universitario de Enfermedades Tropicales y Salud Pública de Canarias (CIBICAN), Universidad de La Laguna, Tenerife, Spain.
[Ti] Título:Genome-wide association study in Spanish identifies ADAM metallopeptidase with thrombospondin type 1 motif, 9 (ADAMTS9), as a novel asthma susceptibility gene.
[So] Source:J Allergy Clin Immunol;137(3):964-6, 2016 Mar.
[Is] ISSN:1097-6825
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Proteínas ADAM/genética
Asma/genética
Grupo com Ancestrais do Continente Europeu/genética
Predisposição Genética para Doença
Estudo de Associação Genômica Ampla
[Mh] Termos MeSH secundário: Proteína ADAMTS9
Estudos de Casos e Controles
Estudos de Associação Genética
Seres Humanos
Polimorfismo de Nucleotídeo Único
Espanha
[Pt] Tipo de publicação:LETTER; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 3.4.24.- (ADAM Proteins); EC 3.4.24.- (ADAMTS9 Protein); EC 3.4.24.- (ADAMTS9 protein, human)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170103
[Lr] Data última revisão:
170103
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:151202
[St] Status:MEDLINE


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[PMID]:26503507
[Au] Autor:Steele MP; Luna LG; Coldren CD; Murphy E; Hennessy CE; Heinz D; Evans CM; Groshong S; Cool C; Cosgrove GP; Brown KK; Fingerlin TE; Schwarz MI; Schwartz DA; Yang IV
[Ad] Endereço:Department of Medicine, Vanderbilt University, Nashville, TN, USA.
[Ti] Título:Relationship between gene expression and lung function in Idiopathic Interstitial Pneumonias.
[So] Source:BMC Genomics;16:869, 2015 Oct 26.
[Is] ISSN:1471-2164
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Idiopathic interstitial pneumonias (IIPs) are a group of heterogeneous, somewhat unpredictable diseases characterized by progressive scarring of the interstitium. Since lung function is a key determinant of survival, we reasoned that the transcriptional profile in IIP lung tissue would be associated with measures of lung function, and could enhance prognostic approaches to IIPs. RESULTS: Using gene expression profiling of 167 lung tissue specimens with IIP diagnosis and 50 control lungs, we identified genes whose expression is associated with changes in lung function (% predicted FVC and % predicted DLCO) modeled as categorical (severe vs mild disease) or continuous variables while adjusting for smoking status and IIP subtype; false discovery rate (FDR) approach was used to correct for multiple comparisons. This analysis identified 58 transcripts that are associated with mild vs severe disease (categorical analysis), including those with established role in fibrosis (ADAMTS4, ADAMTS9, AGER, HIF-1α, SERPINA3, SERPINE2, and SELE) as well as novel IIP candidate genes such as rhotekin 2 (RTKN2) and peptidase inhibitor 15 (PI15). Protein-protein interactome analysis of 553 genes whose expression is significantly associated with lung function when modeled as continuous variables demonstrates that more severe presentation of IIPs is characterized by an increase in cell cycle progression and apoptosis, increased hypoxia, and dampened innate immune response. Our findings were validated in an independent cohort of 131 IIPs and 40 controls at the mRNA level and for one gene (RTKN2) at the protein level by immunohistochemistry in a subset of samples. CONCLUSIONS: We identified commonalities and differences in gene expression among different subtypes of IIPs. Disease progression, as characterized by lower measures of FVC and DLCO, results in marked changes in expression of novel and established genes and pathways involved in IIPs. These genes and pathways represent strong candidates for biomarker studies and potential therapeutic targets for IIP severity.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica
Pneumonias Intersticiais Idiopáticas/genética
Pneumonias Intersticiais Idiopáticas/fisiopatologia
Pulmão/fisiopatologia
Proteínas/genética
[Mh] Termos MeSH secundário: Proteínas ADAM/genética
Proteínas ADAM/metabolismo
Proteína ADAMTS4
Proteína ADAMTS9
Adulto
Idoso
Selectina E/genética
Selectina E/metabolismo
Feminino
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/genética
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Peptídeos e Proteínas de Sinalização Intracelular/genética
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Masculino
Meia-Idade
Pró-Colágeno N-Endopeptidase/genética
Pró-Colágeno N-Endopeptidase/metabolismo
Receptor para Produtos Finais de Glicação Avançada/genética
Receptor para Produtos Finais de Glicação Avançada/metabolismo
Serpina E2/genética
Serpina E2/metabolismo
Serpinas/genética
Serpinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (E-Selectin); 0 (HIF1A protein, human); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Intracellular Signaling Peptides and Proteins); 0 (Proteins); 0 (RTKN2 protein, human); 0 (Receptor for Advanced Glycation End Products); 0 (SELE protein, human); 0 (SERPINA3 protein, human); 0 (SERPINE2 protein, human); 0 (Serpin E2); 0 (Serpins); EC 3.4.24.- (ADAM Proteins); EC 3.4.24.- (ADAMTS9 Protein); EC 3.4.24.- (ADAMTS9 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:1607
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151028
[St] Status:MEDLINE
[do] DOI:10.1186/s12864-015-2102-3


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[PMID]:26027930
[Au] Autor:Nandadasa S; Nelson CM; Apte SS
[Ad] Endereço:Department of Biomedical Engineering, Cleveland Clinic Lerner Research Institute, Cleveland, OH 44195, USA.
[Ti] Título:ADAMTS9-Mediated Extracellular Matrix Dynamics Regulates Umbilical Cord Vascular Smooth Muscle Differentiation and Rotation.
[So] Source:Cell Rep;11(10):1519-28, 2015 Jun 16.
[Is] ISSN:2211-1247
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Despite the significance for fetal nourishment in mammals, mechanisms of umbilical cord vascular growth remain poorly understood. Here, the secreted metalloprotease ADAMTS9 is shown to be necessary for murine umbilical cord vascular development. Restricting it to the cell surface using a gene trap allele, Adamts9(Gt), impaired umbilical vessel elongation and radial growth via reduced versican proteolysis and accumulation of extracellular matrix (ECM). Both Adamts9(Gt) and conditional Adamts9 deletion revealed that ADAMTS9 produced by mesenchymal cells acted non-autonomously to regulate smooth muscle cell (SMC) proliferation, differentiation, and orthogonal reorientation during growth of the umbilical vasculature. In Adamts9(Gt/Gt), we observed interference with PDGFRß signaling via the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway, which regulates cytoskeletal dynamics during SMC rotation. In addition, we observed disrupted Shh signaling and perturbed orientation of the mesenchymal primary cilium. Thus, ECM dynamics is a major influence on umbilical vascular SMC fate, with ADAMTS9 acting as its principal mediator.
[Mh] Termos MeSH primário: Proteínas ADAM/metabolismo
Matriz Extracelular/metabolismo
Músculo Liso Vascular/metabolismo
Cordão Umbilical/metabolismo
[Mh] Termos MeSH secundário: Proteína ADAMTS9
Animais
Diferenciação Celular/fisiologia
Células Cultivadas
Embrião de Mamíferos
Células-Tronco Embrionárias/citologia
Células-Tronco Embrionárias/metabolismo
Feminino
Masculino
Camundongos
Camundongos Transgênicos
Músculo Liso Vascular/citologia
Transdução de Sinais
Cordão Umbilical/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 3.4.24.- (ADAM Proteins); EC 3.4.24.- (ADAMTS9 Protein); EC 3.4.24.- (Adamts9 protein, mouse)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150602
[St] Status:MEDLINE



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