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[PMID]:28890348
[Au] Autor:Li M; Liu Q; Lei J; Wang X; Chen X; Ding Y
[Ad] Endereço:Department of Clinical Research Center, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
[Ti] Título:MiR-362-3p inhibits the proliferation and migration of vascular smooth muscle cells in atherosclerosis by targeting ADAMTS1.
[So] Source:Biochem Biophys Res Commun;493(1):270-276, 2017 Nov 04.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Atherosclerosis is a progressive condition of the large arteries that can cause coronary artery disease (CAD). Growing amounts of evidence have indicated that microRNAs (miRNAs, miRs) can be used as diagnostic biomarkers in many cellular processes associated with CAD. MiR-362-3p has been implicated in many biological cellular functions. However, little is known about the role of miR-362-3p during atherosclerosis. In the present study, significant downregulation of miR-362-3p was observed in 110 atherosclerotic CAD patients and not in the 84 controls. The upregulation of miR-362-3p was demonstrated to inhibit vascular smooth muscle cell (VSMC) proliferation and migration, and impede the G1/S cell cycle transition. Bioinformatics analysis indicated that a disintegrin and metalloproteinase with thrombospondin motifs 1 (ADAMTS1) was a direct target of miR-362-3p. Subsequent experiments demonstrated that miR-362-3p binds to the 3'-untranslated region (UTR) of ADAMTS1 and decreases its levels of mRNA and protein expression. Overexpression of ADAMTS1 partially restored the miR-362-3p-mediated inhibition of VSMC proliferation, cell cycle, and migration. Upregulation of ADAMTS1 in plasma samples was detected in atherosclerotic CAD patients. Taken together, our findings suggested that miR-362-3p inhibits the proliferation and migration of VSMCs by directly targeting ADAMTS1, which might provide novel insight into the molecular mechanisms underlying the action of miR-362-3p in atherosclerosis.
[Mh] Termos MeSH primário: Proteína ADAMTS1/metabolismo
Aterosclerose/metabolismo
MicroRNAs/metabolismo
Músculo Liso Vascular/metabolismo
Miócitos de Músculo Liso/metabolismo
[Mh] Termos MeSH secundário: Aterosclerose/patologia
Movimento Celular
Proliferação Celular
Células Cultivadas
Seres Humanos
Músculo Liso Vascular/patologia
Miócitos de Músculo Liso/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN362 microRNA, human); 0 (MicroRNAs); EC 3.4.24.- (ADAMTS1 Protein); EC 3.4.24.- (ADAMTS1 protein, human)
[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:170912
[St] Status:MEDLINE


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[PMID]:28674292
[Au] Autor:Hirohata S; Inagaki J; Ohtsuki T
[Ad] Endereço:Department of Medical Technology, Graduate School of Health Sciences, Okayama University.
[Ti] Título:Diverse Functions of a Disintegrin and Metalloproteinase with Thrombospondin Motif-1.
[So] Source:Yakugaku Zasshi;137(7):811-814, 2017.
[Is] ISSN:1347-5231
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:A disintegrin and metalloproteinase with thrombospondin motif-1 (ADAMTS1) was initially cloned from a colon cachexia cell line. In the last 20 years, novel matrix metalloproteinase (MMP) genes were found, and in addition to their original members (MMPs and membrane-type MMPs), the current MMP family contains a disintegrin and metalloproteinases (ADAMs) and ADAMTS. ADAM and ADAMTS play essential roles in organogenesis as well as various diseases including osteoarthritis. ADAMTS has 19 members and can be divided into several groups according to their substrates. ADAMTS1, the first member of ADAMTS identified, is located on chromosome 21 very close to another ADAMTS member, ADAMTS5. Interestingly, ADAMTS1 is not highly expressed in normal tissues. One stimulation such as inflammation quickly induces ADAMTS1 expression. We found that hypoxia induced ADAMTS1 expression in endothelial cells, and serum ADAMTS1 levels were elevated in acute myocardial infarction patients. Once the artery was reperfused, the serum ADAMTS1 level quickly returned to the normal level. We also found that ADAMTS1 has specific roles in angiogenesis and lymphangiogenesis, and these functions were not related to its protease activity. It is also interesting that ADAMTS1 is likely to have a unique role in the tumor microenvironment. We also analyzed ADAMTS1-deficient mice and the results suggested that ADAMTS1 has diverse biological functions.
[Mh] Termos MeSH primário: Proteína ADAMTS1/fisiologia
[Mh] Termos MeSH secundário: Proteína ADAMTS1/classificação
Proteína ADAMTS1/genética
Animais
Matriz Extracelular/metabolismo
Expressão Gênica
Seres Humanos
Linfangiogênese/genética
Camundongos
Infarto do Miocárdio/genética
Neovascularização Fisiológica/genética
Organogênese/genética
Osteoartrite/genética
Microambiente Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
EC 3.4.24.- (ADAMTS1 Protein)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170705
[St] Status:MEDLINE
[do] DOI:10.1248/yakushi.16-00236-4


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[PMID]:28570682
[Au] Autor:Vorkapic E; Folkesson M; Magnell K; Bohlooly-Y M; Länne T; Wågsäter D
[Ad] Endereço:Division of Drug Research, Department of Medical and Health Sciences, Linköping University, Linköping, Sweden.
[Ti] Título:ADAMTS-1 in abdominal aortic aneurysm.
[So] Source:PLoS One;12(6):e0178729, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Extracellular matrix degradation is a hallmark of abdominal aortic aneurysm (AAA). Among proteases that are capable of degrading extracellular matrix are a disintegrin and metalloproteases with thrombospondin motifs (ADAMTS). Pathogenesis of these proteases in AAA has not been investigated until date. METHODS AND RESULTS: Human aneurysmal and control aortas were collected and analyzed with RT-PCR measuring the ADAMTS-1, 4,5,6,8,9,10,13,17 and ADAMTSL-1. Expression of a majority of the investigated ADAMTS members on mRNA level was decreased in aneurysm compared to control aorta. ADAMTS-1 was one of the members that was reduced most. Protein analysis using immunohistochemistry and western blot for localization and expression of ADAMTS-1 revealed that ADAMTS-1 was present predominantly in areas of SMCs and macrophages in aneurysmal aorta and higher expressed in AAA compared to control aortas. The role of ADAMTS-1 in AAA disease was further examined using ADAMTS-1 transgenic/apoE-/- mice with the experimental angiotensin II induced aneurysmal model. Transgenic mice overexpressing ADAMTS-1 showed to be similar to ADAMTS-1 wild type mice pertaining collagen, elastin content and aortic diameter. CONCLUSION: Several of the ADAMTS members, and especially ADAMTS-1, are down regulated at mRNA level in AAA, due to unknown mechanisms, at the same time ADAMTS-1 protein is induced. The cleavage of its substrates, don't seem to be crucial for the pathogenesis of AAA but rather more important in the development of thoracic aortic aneurysm and atherosclerosis as shown in previous studies.
[Mh] Termos MeSH primário: Proteína ADAMTS1/metabolismo
Aneurisma da Aorta Abdominal/metabolismo
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Masculino
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.4.24.- (ADAMTS1 Protein); EC 3.4.24.- (ADAMTS1 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170602
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178729


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[PMID]:28067899
[Au] Autor:Oller J; Méndez-Barbero N; Ruiz EJ; Villahoz S; Renard M; Canelas LI; Briones AM; Alberca R; Lozano-Vidal N; Hurlé MA; Milewicz D; Evangelista A; Salaices M; Nistal JF; Jiménez-Borreguero LJ; De Backer J; Campanero MR; Redondo JM
[Ad] Endereço:Gene regulation in cardiovascular remodeling and inflammation group, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
[Ti] Título:Nitric oxide mediates aortic disease in mice deficient in the metalloprotease Adamts1 and in a mouse model of Marfan syndrome.
[So] Source:Nat Med;23(2):200-212, 2017 Feb.
[Is] ISSN:1546-170X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Heritable thoracic aortic aneurysms and dissections (TAAD), including Marfan syndrome (MFS), currently lack a cure, and causative mutations have been identified for only a fraction of affected families. Here we identify the metalloproteinase ADAMTS1 and inducible nitric oxide synthase (NOS2) as therapeutic targets in individuals with TAAD. We show that Adamts1 is a major mediator of vascular homeostasis, given that genetic haploinsufficiency of Adamts1 in mice causes TAAD similar to MFS. Aortic nitric oxide and Nos2 levels were higher in Adamts1-deficient mice and in a mouse model of MFS (hereafter referred to as MFS mice), and Nos2 inactivation protected both types of mice from aortic pathology. Pharmacological inhibition of Nos2 rapidly reversed aortic dilation and medial degeneration in young Adamts1-deficient mice and in young or old MFS mice. Patients with MFS showed elevated NOS2 and decreased ADAMTS1 protein levels in the aorta. These findings uncover a possible causative role for the ADAMTS1-NOS2 axis in human TAAD and warrant evaluation of NOS2 inhibitors for therapy.
[Mh] Termos MeSH primário: Proteína ADAMTS1/genética
Aneurisma Dissecante/genética
Aorta/metabolismo
Aneurisma Aórtico/genética
Síndrome de Marfan/genética
Óxido Nítrico Sintase Tipo II/genética
Óxido Nítrico/metabolismo
[Mh] Termos MeSH secundário: Proteína ADAMTS1/metabolismo
Adulto
Idoso
Aneurisma Dissecante/metabolismo
Animais
Aorta/efeitos dos fármacos
Aneurisma Aórtico/metabolismo
Aneurisma da Aorta Torácica/genética
Aneurisma da Aorta Torácica/metabolismo
Modelos Animais de Doenças
Inibidores Enzimáticos/farmacologia
Feminino
Fibrilina-1/genética
Técnicas de Silenciamento de Genes
Haploinsuficiência
Seres Humanos
Immunoblotting
Masculino
Síndrome de Marfan/metabolismo
Camundongos
Meia-Idade
NG-Nitroarginina Metil Éster/farmacologia
Óxido Nítrico Sintase Tipo II/antagonistas & inibidores
Óxido Nítrico Sintase Tipo II/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Fbn1 protein, mouse); 0 (Fibrillin-1); 31C4KY9ESH (Nitric Oxide); EC 1.14.13.39 (NOS2 protein, human); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, mouse); EC 3.4.24.- (ADAMTS1 Protein); EC 3.4.24.- (ADAMTS1 protein, human); EC 3.4.24.- (Adamts1 protein, mouse); V55S2QJN2X (NG-Nitroarginine Methyl Ester)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170110
[St] Status:MEDLINE
[do] DOI:10.1038/nm.4266


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[PMID]:27908842
[Au] Autor:Özler S; Öztas E; Tokmak A; Ergin M; Kuru Pekcan M; Gümüs Güler B; Yakut HI; Yilmaz N
[Ad] Endereço:Zekai Tahir Burak Women's Health Training and Research Hospital, Clinic of Perinatology, Ankara, Turkey Phone: +90 312 306 50 00 E-mail: sibel2ozler@gmail.com.
[Ti] Título:Role of Versican and ADAMTS-1 in Polycystic Ovary Syndrome.
[So] Source:J Clin Res Pediatr Endocrinol;9(1):24-30, 2017 Mar 01.
[Is] ISSN:1308-5735
[Cp] País de publicação:Turkey
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: ADAMTS-1 is a matrix metalloproteinase which cleaves versican in the cumulus oocyte complex under the effect of luteinizing hormone surge in the periovulatory period. Altered levels may have a role in the pathogenesis of polycystic ovary syndrome (PCOS). We aimed to determine the serum versican and ADAMTS-1 (a disintegrin and metalloproteinase with thrombospondin motif-1) levels in PCOS patients and compare the results with healthy controls. METHODS: Thirty-eight patients with PCOS and forty healthy controls aged between 15 and 22 years were included in the study. They were sampled according to their basal hormone, serum versican, and ADAMTS-1 levels. Serum versican and ADAMTS-1 levels were measured by enzyme-linked immunosorbent assay. A multivariate logistic regression model was used to identify the independent risk factors of PCOS. RESULTS: Serum versican levels were significantly decreased in the PCOS group when compared with the controls. The best versican cut-off value for PCOS was calculated to be 33.65 with 76.74% sensitivity and 52.94% specificity. Serum versican levels, homeostasis model assessment of insulin resistance index, a Ferriman-Gallwey score higher than 8, and oligomenorrhea were the strongest predictors of PCOS. Serum versican levels were significantly decreased in PCOS patients. Besides, serum ADAMTS-1 and versican levels were significantly and positively correlated with each other. CONCLUSION: Serum versican levels were significantly decreased in patients with PCOS. This suggests a possible role of versican in ovulatory dysfunction and in the pathogenesis of PCOS.
[Mh] Termos MeSH primário: Proteína ADAMTS1/sangue
Síndrome do Ovário Policístico/sangue
Medição de Risco/métodos
Versicanas/sangue
[Mh] Termos MeSH secundário: Adolescente
Índice de Massa Corporal
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Resistência à Insulina
Modelos Logísticos
Análise Multivariada
Oligomenorreia/sangue
Oligomenorreia/diagnóstico
Síndrome do Ovário Policístico/diagnóstico
Curva ROC
Valores de Referência
Medição de Risco/estatística & dados numéricos
Fatores de Risco
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (VCAN protein, human); 126968-45-4 (Versicans); EC 3.4.24.- (ADAMTS1 Protein); EC 3.4.24.- (ADAMTS1 protein, human)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170707
[Lr] Data última revisão:
170707
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161203
[St] Status:MEDLINE
[do] DOI:10.4274/jcrpe.3414


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[PMID]:27844209
[Au] Autor:Karakose M; Caliskan M; Arslan MS; Demirci T; Karakose S; Cakal E
[Ad] Endereço:Department of Endocrinology and Metabolism, Diskapi Yildirim Beyazit Training and Research Hospital, Ankara, Turkey. meliakarakose@yahoo.com.
[Ti] Título:The impact of parathyroidectomy on serum ADAMTS1, ADAMTS4 levels, insulin resistance, and subclinical cardiovascular disease in primary hyperparathyroidism.
[So] Source:Endocrine;55(1):283-288, 2017 Jan.
[Is] ISSN:1559-0100
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Primary hyperparathyroidism has been associated with increased incidence of morbidity and mortality of the cardiovascular system. The etiopathogenetic mechanisms underlying this association are still not completely clear. Accumulating evidence suggested that a disintegrin and metalloproteinase with thrombospondin-like motifs (ADAMTS) has a role in the development of inflammation and atherosclerosis. In this study, we aimed to determine whether there is a change in serum levels of ADAMTS1, ADAMTS4, carotid intima-media thickness, and cardiovascular risk score after the surgery and also whether there is a relationship between ADAMTS levels and cardiovascular risk score in hypercalcemic primary hyperparathyroidism patients. METHODS: The study included the 48 consecutive newly diagnosed patients with primary hyperparathyroidism. The patients were evaluated before and six months after parathyroidectomy. The Framingham score is used to calculate cardiovascular risk. Serum ADAMTS levels were determined by a human enzyme-linked immunoassay in all subjects. RESULTS: The fasting glucose, fasting insulin levels and HOMA values were decreased significantly in all patients after surgery compared to the pretreatment values (p < 0.05). ADAMTS1, ADAMTS4, and carotid intima-media thickness levels were significantly lower after surgical correction of primary hyperparathyroidism compared to the preoperative values (p < 0.05). cardiovascular risk score was decreased after parathyroidectomy however, the difference were not statistical significant (p > 0.05). There were statistically significant relationship between cardiovascular risk score and waist/hip ratio, calcium, LDL-cholesterol, carotid intima-media thickness, ADAMTS4 values. CONCLUSION: Based on the results of the present study, fasting glucose, fasting insulin levels, ADAMTS1, ADAMTS4, and carotid intima-media thickness might be an additional parameters during the management of patients with primary hyperparathyroidism, since these factors might improve after surgery.
[Mh] Termos MeSH primário: Proteína ADAMTS1/sangue
Proteína ADAMTS4/sangue
Doenças Cardiovasculares/sangue
Hiperparatireoidismo Primário/cirurgia
Resistência à Insulina/fisiologia
[Mh] Termos MeSH secundário: Adulto
Glicemia
Espessura Intima-Media Carotídea
Feminino
Seres Humanos
Hiperparatireoidismo Primário/sangue
Masculino
Meia-Idade
Hormônio Paratireóideo/sangue
Paratireoidectomia
Fatores de Risco
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Parathyroid Hormone); EC 3.4.24.- (ADAMTS1 Protein); EC 3.4.24.82 (ADAMTS4 Protein)
[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:161116
[St] Status:MEDLINE
[do] DOI:10.1007/s12020-016-1175-3


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[PMID]:25689086
[Au] Autor:Pelisek J; Deutsch L; Ansel A; Pongratz J; Stadlbauer T; Gebhard H; Matevossian E; Eckstein HH
[Ad] Endereço:aDepartment of Vascular and Endovascular Surgery, Klinikum rechts der Isar der Technischen Universitaet Muenchen, Munich bKantonsspital Baselland, Orthopaedics und Traumatology, CH-4410 Liestal cDepartment of Surgery, Munich Transplant Centre, Klinikum rechts der Isar der Technischen Universitaet Muenchen dDZHK (German Centre for Cardiovascular Research), partner site Munich Heart Alliance, Munich, Germany.
[Ti] Título:Expression of a metalloproteinase family of ADAMTS in human vulnerable carotid lesions.
[So] Source:J Cardiovasc Med (Hagerstown);18(1):10-18, 2017 Jan.
[Is] ISSN:1558-2035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIMS: ADAMTS family of metalloproteases (a disintegrin and metalloprotease with thrombospondin motifs) possesses high proteolytic activity especially regarding proteoglycans. Their expression pattern in carotid plaques is as-yet unknown. The aim of the study was therefore the analysis of expression of ADAMTS1, 4, 5, and 13 and their inhibitors TIMP-1 and TIMP-3 in stable and unstable carotid plaques. METHODS: Atherosclerotic plaques were collected from 40 patients (29 men, 11 women, mean age 70 years) undergoing carotid endarterectomy. The specimens were categorized into two groups (stable/unstable) according to Redgrave und Rothwell (The Oxford Plaque Study, 2008). SYBR Green-based real-time PCR, histology, and immunohistochemistry were performed. RESULTS: All ADAMTS tested in our study were expressed in both stable and unstable plaques, especially in smooth muscle cells (SMCs) and macrophages. Analysis of the expression pattern on mRNA level showed significant higher expression of ADAMTS1 in unstable plaques compared with stable plaques (1.7-fold, P = 0.049). The expression of ADAMTS4 and 5 was also increased in unstable lesions; however, these changes were not statistically significant (1.2-fold, P = 0.667 and 1.6-fold, P = 0.077). Expression of TIMP-1 was significantly reduced in unstable plaques compared with stable ones (1.9-fold, P = 0.014). CONCLUSION: SMCs seem to be an important source of ADAMTS analyzed in our study. Furthermore, expression of ADAMTS1 was found to be increased in unstable carotid lesions and might potentially contribute to plaque vulnerability.
[Mh] Termos MeSH primário: Proteína ADAMTS1/genética
Estenose das Carótidas/cirurgia
Placa Aterosclerótica/genética
Placa Aterosclerótica/patologia
Acidente Vascular Cerebral/epidemiologia
[Mh] Termos MeSH secundário: Idoso
Endarterectomia das Carótidas
Feminino
Alemanha
Seres Humanos
Imuno-Histoquímica
Macrófagos/metabolismo
Masculino
Meia-Idade
Miócitos de Músculo Liso/metabolismo
Estudos Retrospectivos
Acidente Vascular Cerebral/etiologia
Inibidor Tecidual de Metaloproteinase-1/genética
Inibidor Tecidual de Metaloproteinase-3/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (TIMP1 protein, human); 0 (TIMP3 protein, human); 0 (Tissue Inhibitor of Metalloproteinase-1); 0 (Tissue Inhibitor of Metalloproteinase-3); EC 3.4.24.- (ADAMTS1 Protein); EC 3.4.24.- (ADAMTS1 protein, human)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150218
[St] Status:MEDLINE


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[PMID]:27916096
[Au] Autor:Liu L; Yin H; Huang M; He J; Yi G; Wang Z; Qian H
[Ad] Endereço:School of Clinical Medicine, Hunan University of Medicine, Huaihua 418000; Department of Respiration, First Affiliated Hospital, Hunan University of Medicine, Huaihua 418000, China.
[Ti] Título:[miR-21 promotes pulmonary fibrosis in rats via down-regulating the expression of ADAMTS-1].
[So] Source:Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi;32(12):1636-1640, 2016 Dec.
[Is] ISSN:1007-8738
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Objective To observe the effect of miR-21 on bleomycin-induced pulmonary fibrosis in rats, and explore the related mechanism. Methods Peripheral blood was collected from idiopathic pulmonary fibrosis (IPF) patients (n=20) and healthy adults (n=20). Fluorescence quantitative real-time PCR was then used to measure miR-21 expression. Forty-five SD rats were randomly divided into control group, miR-21 agomir group and miR-21 antagomir group. Each group included 15 rats. After establishment of pulmonary fibrosis models by intratracheal administration with bleomycin A5, rats in control group, miR-21 agomir group and miR-21 antagomir group were injected at caudal vein with normal saline, miR21 agomir and miR21 antagomir, respectively. All rats were sacrificed on day 28 after modeling. Subsequently, the pulmonary tissues were removed for HE and Masson staining. The mRNA and protein expressions of a disintegrin-like and metalloproteinase with thrombospondin type 1 motif (ADAMTS-1), collagen type 1 (Col1) and collagen type 3 (Col3) were detected by fluorescence quantitative real-time PCR and Western blotting. Serum was separated to examine procollagen type 1 carboxyterminal propeptide (P1CP) and procollagen type 3 aminoterminal propeptide (P3NP) concentrations by ELISA. Results The level of miR-21 in peripheral blood was higher in IPF patients than in healthy adults. The alveolitis and pulmonary fibrosis extent in miR-21 agomir group was heavier than that in the control group. However, the alveolitis and pulmonary fibrosis extent in miR-21 antagomir group was improved when compared with the control group. In comparison with the control group, ADAMTS-1 mRNA and protein expression was significantly downregulated, whereas the mRNA and protein expressions of Col1 and Col3 were significantly upregulated and serum P1CP and P3NP concentrations were elevated in miR-21 agomir group. On the contrary, the level of ADAMTS-1 mRNA and protein expression in miR-21 antagomir group was higher than that in the control group; the levels of Col1 and Col3 mRNA and protein as well as serum P1CP and P3NP concentrations in miR-21 antagomir group were lower than those in the control group. Conclusion miR-21 promotes the progression of bleomycin-induced pulmonary fibrosis in rats. The mechanism is associated with downregulation of ADAMTS-1 expression and subsequent increase of pulmonary Col1 and Col3 contents.
[Mh] Termos MeSH primário: Proteína ADAMTS1/metabolismo
MicroRNAs/metabolismo
Fibrose Pulmonar/metabolismo
[Mh] Termos MeSH secundário: Proteína ADAMTS1/genética
Adulto
Idoso
Animais
Bleomicina/análogos & derivados
Bleomicina/toxicidade
Colágeno Tipo I/metabolismo
Colágeno Tipo III/metabolismo
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Masculino
MicroRNAs/agonistas
MicroRNAs/antagonistas & inibidores
Meia-Idade
Fibrose Pulmonar/induzido quimicamente
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type I); 0 (Collagen Type III); 0 (MIRN21 microRNA, human); 0 (MicroRNAs); 0 (mirn21 microRNA, rat); 11056-06-7 (Bleomycin); 5DY91Y7601 (bleomycetin); EC 3.4.24.- (ADAMTS1 Protein)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170613
[Lr] Data última revisão:
170613
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161206
[St] Status:MEDLINE


  9 / 235 MEDLINE  
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[PMID]:27764205
[Au] Autor:Silva SV; Lima MA; Cella N; Jaeger RG; Freitas VM
[Ad] Endereço:Department of Cell and Developmental Biology, Biomedical Sciences Institute, University of São Paulo, São Paulo, Brazil.
[Ti] Título:ADAMTS-1 Is Found in the Nuclei of Normal and Tumoral Breast Cells.
[So] Source:PLoS One;11(10):e0165061, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Proteins secreted in the extracellular matrix microenvironment (ECM) by tumor cells are involved in cell adhesion, motility, intercellular communication and invasion. The tumor microenvironment is expansively modified and remodeled by proteases, resulting in important changes in both cell-cell and cell-ECM interactions and in the generation of new signals from the cell surface. Metalloproteinases belonging to the ADAMTS (a disintegrin and metalloprotease with thrombospondin motifs) family have been implicated in tissue remodeling events observed in cancer development, growth and progression. Here we investigated the subcellular localization of ADAMTS-1 in normal-like (MCF10-A) and tumoral (MCF7 and MDA-MB-231) human breast cells. ADAMTS-1 is a secreted protease found in the extracellular matrix. However, in this study we show for the first time that ADAMTS-1 is also present in the nuclei and nucleoli of the three mammary cell lines studied here. Our findings indicate that ADAMTS-1 has proteolytic functions in the nucleus through its interaction with aggrecan substrate.
[Mh] Termos MeSH primário: Proteína ADAMTS1/metabolismo
Neoplasias da Mama/enzimologia
Núcleo Celular/enzimologia
[Mh] Termos MeSH secundário: Agrecanas/metabolismo
Linhagem Celular
Feminino
Seres Humanos
Células MCF-7
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aggrecans); EC 3.4.24.- (ADAMTS1 Protein); EC 3.4.24.- (ADAMTS1 protein, human)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170605
[Lr] Data última revisão:
170605
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161021
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0165061


  10 / 235 MEDLINE  
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[PMID]:27667459
[Au] Autor:Liu L; Qian H; Xiao H; He J; Xie M; Wang Z; Long X
[Ad] Endereço:School of Clinical Medicine, Hunan University of Medicine, Huaihua 418000, China.
[Ti] Título:[Emodin alleviates pulmonary fibrosis through inactivation of TGF-ß1/ADAMTS-1 signaling pathway in rats].
[So] Source:Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi;32(10):1342-1346, 2016 Oct.
[Is] ISSN:1007-8738
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Objective To explore the role of transforming growth factor-ß1 (TGF-ß1)/a disintegrin-like and metalloproteinase with thrombospondin type 1 motif (ADAMTS-1) signaling pathway in emodin's anti-pulmonary fibrosis. Methods Sixty SD rats were randomly divided into 6 groups: normal control group, sham-operated group, model group, low-dose emodin intervention group (20 mg/kg), high-dose emodin intervention group (80 mg/kg) and prednisone group (5 mg/kg). Each group included 10 animals. Rats in the latter 4 groups were intratracheally injected with bleomycin A5 to induce pulmonary fibrosis, whereas bleomycin A5 was replaced by normal saline in sham-operated group. From the second day, rats in the low- and high-dose emodin intervention groups were intragastrically treated with 2 mL of 20 and 80 mg/kg emodin, respectively. Rats in the prednisone group were intragastrically administrated with 2 mL of 5 mg/kg prednisone acetate. However, rats in the normal control and sham-operated and model groups were treated with 2 mL of normal saline. All rats were sacrificed on day 28 after modeling. Subsequently, blood and pulmonary tissue specimen were taken. The pathological changes of pulmonary tissues were observed using routine HE and Masson staining. The expressions of TGF-ß1, ADAMTS-1, collagen type 1 (Col1) and Col3 in pulmonary tissues were measured by quantitative real-time PCR and Western blotting. Serum levels of procollagen type 1 carboxy terminal propeptide (P1CP) and procollagen type 3 aminoterminal propeptide (P3NP) were detected by ELISA. Results Compare with the model group, the alveolitis and pulmonary fibrosis extent in each drug-treated group were significantly alleviated. In comparison with normal control group or sham-operated group, the mRNA and protein levels of TGF-ß1, Col1 and Col3 in pulmonary tissues and the serum levels of P1CP and P3NP increased, but the mRNA and protein levels of ADAMTS-1 decreased in model group. After treatment with low- and high-dose emodin or prednisone, the mRNA and protein levels of TGF-ß1, Col1 and Col3 in pulmonary tissues and the serum levels of P1CP and P3NP were significantly downregulated, while the mRNA and protein levels of ADAMTS-1 in pulmonary tissues were significantly upregulated as compared with the model group. Moreover, In comparison with the low-dose emodin intervention group, the above indicators were significantly improved in the high-dose emodin intervention or prednisone group. However, the above indicators were not significantly different between the high-dose emodin intervention group and the prednisone group. Conclusion Increased degradation of Col1 and Col3 in pulmonary tissues due to the inactivation of TGF-ß1/ADAMTS-1 signaling pathway may be a significant mechanism by which emodin protects rats against pulmonary fibrosis.
[Mh] Termos MeSH primário: Proteína ADAMTS1/metabolismo
Medicamentos de Ervas Chinesas/administração & dosagem
Emodina/administração & dosagem
Fibrose Pulmonar/tratamento farmacológico
Transdução de Sinais/efeitos dos fármacos
Fator de Crescimento Transformador beta1/metabolismo
[Mh] Termos MeSH secundário: Proteína ADAMTS1/genética
Animais
Colágeno Tipo I/genética
Colágeno Tipo I/metabolismo
Colágeno Tipo III/genética
Colágeno Tipo III/metabolismo
Seres Humanos
Masculino
Fragmentos de Peptídeos/sangue
Pró-Colágeno/sangue
Fibrose Pulmonar/genética
Fibrose Pulmonar/metabolismo
Ratos
Ratos Sprague-Dawley
Fator de Crescimento Transformador beta1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type I); 0 (Collagen Type III); 0 (Drugs, Chinese Herbal); 0 (Peptide Fragments); 0 (Procollagen); 0 (Transforming Growth Factor beta1); 0 (procollagen Type III-N-terminal peptide); 0 (procollagen type I carboxy terminal peptide); EC 3.4.24.- (ADAMTS1 Protein); EC 3.4.24.- (Adamts1 protein, rat); KA46RNI6HN (Emodin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160927
[St] Status:MEDLINE



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