Base de dados : MEDLINE
Pesquisa : D12.776.260.108.217 [Categoria DeCS]
Referências encontradas : 569 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 57 ir para página                         

  1 / 569 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28784605
[Au] Autor:Seidl MD; Stein J; Hamer S; Pluteanu F; Scholz B; Wardelmann E; Huge A; Witten A; Stoll M; Hammer E; Völker U; Müller FU
[Ad] Endereço:From the Institute of Pharmacology and Toxicology, University of Münster, Germany (M.D.S., J.S., S.H., F.P., B.S., F.U.M.); Department of Genetic Epidemiology, Institute of Human Genetics, University of Münster, Germany (A.H., A.W., M.S.); Gerhard-Domagk-Institute of Pathology, University Hospital M
[Ti] Título:Characterization of the Genetic Program Linked to the Development of Atrial Fibrillation in CREM-IbΔC-X Mice.
[So] Source:Circ Arrhythm Electrophysiol;10(8), 2017 Aug.
[Is] ISSN:1941-3084
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Reduced expression of genes regulated by the transcription factors CREB/CREM (cAMP response element-binding protein/modulator) is linked to atrial fibrillation (AF) susceptibility in patients. Cardiomyocyte-directed expression of the inhibitory CREM isoform CREM-IbΔC-X in transgenic mice (TG) leads to spontaneous-onset AF preceded by atrial dilatation and conduction abnormalities. Here, we characterized the altered gene program linked to atrial remodeling and development of AF in CREM-TG mice. METHODS AND RESULTS: Atria of young (TGy, before AF onset) and old (TGo, after AF onset) TG mice were investigated by mRNA microarray profiling in comparison with age-matched wild-type controls (WTy/WTo). Proteomic alterations were profiled in young mice (8 TGy versus 8 WTy). Annotation of differentially expressed genes revealed distinct differences in biological functions and pathways before and after onset of AF. Alterations in metabolic pathways, some linked to altered peroxisome proliferator-activated receptor signaling, muscle contraction, and ion transport were already present in TGy. Electron microscopy revealed significant loss of sarcomeres and mitochondria and increased collagen and glycogen deposition in TG mice. Alterations in electrophysiological pathways became prominent in TGo, concomitant with altered gene expression of K -channel subunits and ion channel modulators, relevant in human AF. CONCLUSIONS: The most prominent alterations of the gene program linked to CREM-induced atrial remodeling were identified in the expression of genes related to structure, metabolism, contractility, and electric activity regulation, suggesting that CREM transgenic mice are a valuable experimental model for human AF pathophysiology.
[Mh] Termos MeSH primário: Fibrilação Atrial/genética
Modulador de Elemento de Resposta do AMP Cíclico/genética
Modelos Animais de Doenças
Perfilação da Expressão Gênica
Camundongos Transgênicos/genética
[Mh] Termos MeSH secundário: Potenciais de Ação/fisiologia
Animais
Fibrilação Atrial/fisiopatologia
Canais Iônicos/metabolismo
Masculino
Potenciais da Membrana/fisiologia
Camundongos
Miócitos Cardíacos/metabolismo
Técnicas de Patch-Clamp
Receptores Ativados por Proliferador de Peroxissomo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Crem protein, mouse); 0 (Ion Channels); 0 (Peroxisome Proliferator-Activated Receptors); 135844-64-3 (Cyclic AMP Response Element Modulator)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170809
[St] Status:MEDLINE


  2 / 569 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28368536
[Au] Autor:Barbati SA; Colussi C; Bacci L; Aiello A; Re A; Stigliano E; Isidori AM; Grassi C; Pontecorvi A; Farsetti A; Gaetano C; Nanni S
[Ad] Endereço:Institute of Human Physiology, Università Cattolica di Roma, 00168 Rome, Italy.
[Ti] Título:Transcription Factor CREM Mediates High Glucose Response in Cardiomyocytes and in a Male Mouse Model of Prolonged Hyperglycemia.
[So] Source:Endocrinology;158(7):2391-2405, 2017 Jul 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study aims at investigating the epigenetic landscape of cardiomyocytes exposed to elevated glucose levels. High glucose (30 mM) for 72 hours determined some epigenetic changes in mouse HL-1 and rat differentiated H9C2 cardiomyocytes including upregulation of class I and III histone deacetylase protein levels and activity, inhibition of histone acetylase p300 activity, increase in histone H3 lysine 27 trimethylation, and reduction in H3 lysine 9 acetylation. Gene expression analysis focused on cardiotoxicity revealed that high glucose induced markers associated with tissue damage, fibrosis, and cardiac remodeling such as Nexilin (NEXN), versican, cyclic adenosine 5'-monophosphate-responsive element modulator (CREM), and adrenoceptor α2A (ADRA2). Notably, the transcription factor CREM was found to be important in the regulation of cardiotoxicity-associated genes as assessed by specific small interfering RNA and chromatin immunoprecipitation experiments. In CD1 mice, made hyperglycemic by streptozotoicin (STZ) injection, cardiac structural alterations were evident at 6 months after STZ treatment and were associated with a significant increase of H3 lysine 27 trimethylation and reduction of H3 lysine 9 acetylation. Consistently, NEXN, CREM, and ADRA2 expression was significantly induced at the RNA and protein levels. Confocal microscopy analysis of NEXN localization showed this protein irregularly distributed along the sarcomeres in the heart of hyperglycemic mice. This evidence suggested a structural alteration of cardiac Z-disk with potential consequences on contractility. In conclusion, high glucose may alter the epigenetic landscape of cardiac cells. Sildenafil, restoring guanosine 3', 5'-cyclic monophosphate levels, counteracted the increase of CREM and NEXN, providing a protective effect in the presence of hyperglycemia.
[Mh] Termos MeSH primário: Cardiotoxicidade/genética
Modulador de Elemento de Resposta do AMP Cíclico/fisiologia
Glucose/efeitos adversos
Glucose/metabolismo
Hiperglicemia/metabolismo
Hiperglicemia/patologia
Miócitos Cardíacos/metabolismo
[Mh] Termos MeSH secundário: Animais
Cardiotoxicidade/metabolismo
Cardiotoxicidade/patologia
Células Cultivadas
Modulador de Elemento de Resposta do AMP Cíclico/genética
Modelos Animais de Doenças
Embrião de Mamíferos
Epigênese Genética/efeitos dos fármacos
Feminino
Hiperglicemia/genética
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Miócitos Cardíacos/efeitos dos fármacos
Miócitos Cardíacos/patologia
Ratos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Crem protein, mouse); 135844-64-3 (Cyclic AMP Response Element Modulator); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE
[do] DOI:10.1210/en.2016-1960


  3 / 569 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28072703
[Au] Autor:Feng F; Wu J; Gao Z; Yu S; Cui Y
[Ad] Endereço:Department of Urological Surgery, Yantai Yuhuangding Hospital, Yantai, Shandong, China.
[Ti] Título:Screening the key microRNAs and transcription factors in prostate cancer based on microRNA functional synergistic relationships.
[So] Source:Medicine (Baltimore);96(1):e5679, 2017 Jan.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prostate cancer (PC) is a common neoplasm, and metastatic PC remains incurable. The study aims to screen key microRNAs (miRNAs) and transcription factors (TFs) involved in PC.The miRNA expression profile dataset (GSE45604) was downloaded from Gene Expression Omnibus database, including 50 PC and 10 normal specimens. Differentially expressed miRNAs (DEmiRNAs) were identified through limma package in R, and DEmiRNA-DEmiRNA co-regulation network was constructed based on the number of co-regulated target genes. Functional enrichment analysis of co-regulated target genes was performed using clusterProfiler package in R, and miRNA interactions sharing at least 1 functional term were used to construct a DEmiRNA-DEmiRNA functional synergistic network (MFSN). Based on Transcriptional Regulatory Element Database, cancer-related TFs which were co-regulated by DEmiRNAs were utilized to construct a DEmiRNA-TF regulation network.A total of 66 DEmiRNAs were identified, including 7 up-regulated miRNAs with 18,642 target genes and 59 down-regulated miRNAs with 130,694 target genes. Then, the DEmiRNA-DEmiRNA co-regulation network was constructed, including 66 DEmiRNAs and 2024 co-regulation relationships. In MFSN, hsa-miR-1184, hsa-miR-1207-5p, and hsa-miR-24 had significant functional synergistic relationships. The DEmiRNA-TF network contained 6 up-regulated DEmiRNAs and 4 of them were highlighted, as hsa-miR-1184, hsa-miR-1207-5p, hsa-miR-182, and hsa-miR-183. In subnetwork of the 4 miRNAs, peroxisome proliferative activated receptor, alpha (PPARA) and cyclic AMP-responsive element modulator (CREM) were the critical regulated TFs.Four up-regulated miRNAs (hsa-miR-1207-5p, hsa-miR-1184, hsa-miR-182, and hsa-miR-183) and 2 TFs (PPARA and CREM) were identified as key regulators in PC progression. The above 4 miRNAs might participate in PC progression by targeting PPARA and CREM.
[Mh] Termos MeSH primário: Regulação Neoplásica da Expressão Gênica
MicroRNAs/genética
Neoplasias da Próstata/genética
Fatores de Transcrição/genética
[Mh] Termos MeSH secundário: Biologia Computacional
Modulador de Elemento de Resposta do AMP Cíclico/genética
Bases de Dados Genéticas
Regulação para Baixo
Expressão Gênica
Perfilação da Expressão Gênica
Seres Humanos
Masculino
PPAR alfa/genética
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CREM protein, human); 0 (MIRN1184 microRNA, human); 0 (MIRN1207 microRNA, human); 0 (MIRN183 microRNA, human); 0 (MicroRNAs); 0 (Mirn182 microRNA, human); 0 (PPAR alpha); 0 (Transcription Factors); 135844-64-3 (Cyclic AMP Response Element Modulator)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170224
[Lr] Data última revisão:
170224
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170111
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000005679


  4 / 569 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28009602
[Au] Autor:Kao YC; Sung YS; Zhang L; Chen CL; Vaiyapuri S; Rosenblum MK; Antonescu CR
[Ad] Endereço:*Department of Pathology, Shuang Ho Hospital, Taipei Medical University, Taipei, Taiwan †Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY ‡Department of Musculoskeletal Pathology, The Royal Orthopaedic Hospital NHS Foundation Trust, Birmingham, UK.
[Ti] Título:EWSR1 Fusions With CREB Family Transcription Factors Define a Novel Myxoid Mesenchymal Tumor With Predilection for Intracranial Location.
[So] Source:Am J Surg Pathol;41(4):482-490, 2017 Apr.
[Is] ISSN:1532-0979
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recurrent gene fusions involving EWSR1 with members of the cAMP response element binding protein (CREB) family (ATF1 and CREB1) have been reported in a diverse group of tumors including angiomatoid fibrous histiocytoma (AFH), soft tissue and gastrointestinal clear cell sarcoma, primary pulmonary myxoid sarcoma, and hyalinizing clear cell carcinoma of salivary gland. We have recently encountered a group of 5 myxoid mesenchymal tumors positive for EWSR1 fusions with one of the CREB family member (ATF1, CREB1, and CREM), with histologic features distinct from any of the previously described pathologic entities. Tumors occurred in children or young adults (12 to 23 y; mean, 18 y), with equal sex distribution. All except 1 were intracranial (intra-axial, 2; meningeal, 2), whereas 1 was perirectal. Histologically, the tumors were well circumscribed, often lobulated, composed of uniform ovoid to round cells, and arranged in cord-like or reticular structures in a myxoid background. All except 1 displayed unique sunburst amianthoid fibers. Immunohistochemically, tumors were positive for epithelial membrane antigen (5/5; 4 focal, 1 diffuse) and desmin (3/5). A novel EWSR1-CREM fusion was identified by RNA sequencing in the perirectal tumor, which was further confirmed by fluorescence in situ hybridization (FISH) and reverse transcription-polymerase chain reaction (RT-PCR). A second case with similar EWSR1-CREM fusion was identified by RT-PCR and FISH in a meningeal tumor. The remaining cases studied by FISH showed the presence of EWSR1-CREB1 fusion in 2 cases and EWSR1-ATF1 in 1. In conclusion, we report a distinct group of myxoid mesenchymal neoplasms occurring in children or young adults with a predilection for intracranial locations. Although the immunoprofile [epithelial membrane antigen (EMA), desmin] and the fusion type raise the possibility of a myxoid AFH, none of the typical histologic findings of AFH were present, suggesting a novel entity.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/genética
Neoplasias Encefálicas/genética
Proteínas de Ligação a Calmodulina/genética
Modulador de Elemento de Resposta do AMP Cíclico/genética
Fusão Gênica
Proteínas de Fusão Oncogênicas/genética
Proteínas de Ligação a RNA/genética
Neoplasias Retais/genética
Neoplasias de Tecidos Moles/genética
[Mh] Termos MeSH secundário: Adolescente
Biomarcadores Tumorais/análise
Biópsia
Neoplasias Encefálicas/química
Neoplasias Encefálicas/patologia
Criança
Feminino
Seres Humanos
Imuno-Histoquímica
Hibridização in Situ Fluorescente
Masculino
Proteína EWS de Ligação a RNA
Neoplasias Retais/química
Neoplasias Retais/patologia
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Análise de Sequência de RNA
Neoplasias de Tecidos Moles/química
Neoplasias de Tecidos Moles/patologia
Células Estromais/química
Células Estromais/patologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CREM protein, human); 0 (Calmodulin-Binding Proteins); 0 (EWSR1 protein, human); 0 (EWSR1-ATF1 fusion protein, human); 0 (EWSR1-CREB1 fusion protein, human); 0 (Oncogene Proteins, Fusion); 0 (RNA-Binding Protein EWS); 0 (RNA-Binding Proteins); 135844-64-3 (Cyclic AMP Response Element Modulator)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161224
[St] Status:MEDLINE
[do] DOI:10.1097/PAS.0000000000000788


  5 / 569 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27822872
[Au] Autor:Greco SJ; Yehia G; Potian JA; Molina CA; Rameshwar P
[Ad] Endereço:Department of Medicine, Division of Hematology-Oncology, New Jersey Medical School, Rutgers School of Biomedical Health Science, Newark, NJ, 07103, USA.
[Ti] Título:Constitutive Expression of Inducible Cyclic Adenosine Monophosphate Early Repressor (ICER) in Cycling Quiescent Hematopoietic Cells: Implications for Aging Hematopoietic Stem Cells.
[So] Source:Stem Cell Rev;13(1):116-126, 2017 Feb.
[Is] ISSN:1558-6804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Despite extensive insights on the interaction between hematopoietic stem cells (HSCs) and the supporting bone marrow (BM) stroma in hematopoietic homeostasis there remains unanswered questions on HSC regulation. We report on the mechanism by which HSCs attain cycling quiescence by addressing a role for inducible cyclic AMP early repressor (ICER). ICER negatively transcriptional regulators of cAMP activators such as CREM and CREB. These activators can be induced by hematopoietic stimulators such as cytokines. We isolated subsets of hematopoietic cells from ten healthy donors: CD34 CD38 /c-kit (primitive progenitor), CD34 CD38 /c-kit (mature progenitor) and CD34 CD38 /c-kit (differentiated lineage-). The relative maturity of the progenitors were verified in long-term culture initiating assay. Immunoprecipitation indicated the highest level of ICER in the nuclear extracts of CD34 /CD38 cells. Phospho (p)-CREM was also present suggesting a balance between ICER and p-CREM in HSC. ICER seems to be responsible for decrease in G1 transition, based on reduced Cdk4 protein, decreased proliferation and functional studies with propidium iodide. There were no marked changes in the cycling inhibitors, p15 and p-Rb, suggesting that ICER may act independently of other cycling inhibitors. The major effects of ICER were validated with BM mononuclear cells (BMNCs) in which ICER was ectopically expressed, and with BMNCs resistant to 5-fluorouracil- or cyclophosphamide. In total, this study ascribes a novel role for ICER in G1 checkpoint regulation in HSCs. These findings are relevant to gene therapy that require engineering of HSCs, age-related disorders that are associated with hematopoietic dysfunction and other hematological disorders.
[Mh] Termos MeSH primário: Ciclo Celular/genética
Modulador de Elemento de Resposta do AMP Cíclico/genética
Expressão Gênica
Células-Tronco Hematopoéticas/metabolismo
[Mh] Termos MeSH secundário: ADP-Ribosil Ciclase 1/metabolismo
Envelhecimento/genética
Envelhecimento/metabolismo
Antígenos CD34/metabolismo
Western Blotting
Diferenciação Celular/efeitos dos fármacos
Diferenciação Celular/genética
Células Cultivadas
Modulador de Elemento de Resposta do AMP Cíclico/metabolismo
Ciclofosfamida/farmacologia
Fluoruracila/farmacologia
Células-Tronco Hematopoéticas/citologia
Seres Humanos
Imunossupressores/farmacologia
Proteínas Proto-Oncogênicas c-kit/metabolismo
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD34); 0 (CREM protein, human); 0 (Immunosuppressive Agents); 135844-64-3 (Cyclic AMP Response Element Modulator); 8N3DW7272P (Cyclophosphamide); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit); EC 3.2.2.6 (ADP-ribosyl Cyclase 1); U3P01618RT (Fluorouracil)
[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:161109
[St] Status:MEDLINE
[do] DOI:10.1007/s12015-016-9701-5


  6 / 569 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27686093
[Au] Autor:Kuttkat N; Mohs A; Ohl K; Hooiveld G; Longerich T; Tenbrock K; Cubero FJ; Trautwein C
[Ad] Endereço:Department of Internal Medicine III, University Hospital RWTH Aachen, Aachen, Germany.
[Ti] Título:Hepatic overexpression of cAMP-responsive element modulator α induces a regulatory T-cell response in a murine model of chronic liver disease.
[So] Source:Gut;66(5):908-919, 2017 May.
[Is] ISSN:1468-3288
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Th17 cells are a subset of CD4 T-helper cells characterised by interleukin 17 (IL-17) production, a cytokine that plays a crucial role in inflammation-associated diseases. The cyclic AMP-responsive element modulator-α (CREMα) is a central mediator of T-cell pathogenesis, which contributes to increased IL-17 expression in patients with autoimmune disorders. Since an increased Th17 response is associated with a poor prognosis in patients with chronic liver injury, we investigated the relevance of Th17 cells for chronic liver disease (CLD) and hepatocarcinogenesis. DESIGN: Transgenic mice overexpressing CREMα were crossed with hepatocyte-specific Nemo knockout mice (Nemo ) to generate Nemo /CREMα mice. The impact of CREMα on CLD progression was examined. Additionally, soft agar colony formation assays, in vitro studies, adoptive transfer of bone marrow-derived cells (BMDCs) and T cells, and gene arrays in T cells were performed. RESULTS: 8-week-old Nemo /CREMα mice presented significantly decreased transaminase levels, concomitant with reduced numbers of CD11b dendritic cells and CD8 T cells. CREMα overexpression in Nemo mice was associated with significantly reduced hepatic fibrogenesis and carcinogenesis at 52 weeks. Interestingly, hepatic stellate cell-derived retinoic acid induced a regulatory T-cell (Treg) phenotype in CREMα hepatic T cells. Moreover, simultaneous adoptive transfer of BMDCs and T cells from CREMα into Nemo mice ameliorated markers of liver injury and hepatitis. CONCLUSIONS: Our results demonstrate that overexpression of CREMα in T cells changes the inflammatory milieu, attenuating initiation and progression of CLD. Unexpectedly, our study indicates that CREMα transgenic T cells shift chronic inflammation in Nemo livers towards a protective Treg response.
[Mh] Termos MeSH primário: Modulador de Elemento de Resposta do AMP Cíclico/genética
Hepatite/imunologia
Neoplasias Hepáticas/imunologia
Linfócitos T/imunologia
Células Th17/imunologia
[Mh] Termos MeSH secundário: Alanina Transaminase/sangue
Animais
Aspartato Aminotransferases/sangue
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos
Linhagem Celular Tumoral
Transformação Celular Neoplásica
Doença Crônica
Modulador de Elemento de Resposta do AMP Cíclico/metabolismo
Células Dendríticas/imunologia
Modelos Animais de Doenças
Progressão da Doença
Fatores de Transcrição Forkhead/metabolismo
Hepatite/genética
Peptídeos e Proteínas de Sinalização Intracelular/genética
Cirrose Hepática/imunologia
Contagem de Linfócitos
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Linfócitos T/metabolismo
Linfócitos T Reguladores/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Intracellular Signaling Peptides and Proteins); 0 (NEMO protein, mouse); 135844-64-3 (Cyclic AMP Response Element Modulator); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.6.1.2 (Alanine Transaminase)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161001
[St] Status:MEDLINE
[do] DOI:10.1136/gutjnl-2015-311119


  7 / 569 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27234251
[Au] Autor:Zhang J; Zhu Y; Liang C; Qie M; Niu R; Sun Z; Wang J; Wang J
[Ad] Endereço:Shanxi Key Laboratory of Ecological Animal Science and Environmental Veterinary Medicine, Shanxi Agricultural University, Taigu, Shanxi, 030801, China. Jianhaiz@163.com.
[Ti] Título:Effects of Fluoride on Expression of P450, CREM and ACT Proteins in Rat Testes.
[So] Source:Biol Trace Elem Res;175(1):156-160, 2017 Jan.
[Is] ISSN:1559-0720
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Fluoride (F) is an essential trace element that humans and animals ingest from water, air, and fluoride-containing products; however, excessive fluoride absorption can damage a variety of organs and tissues, including the male reproductive system. Our previous studies found that fluoride exposure lowered sperm quality and interfered with spermatogenesis; however, the exact mechanism remained unclear. Proteins cytochrome P450 (P450), cAMP-responsive element modulator (CREM), and activator of CREM in testis (ACT) play the key roles in spermatogenesis and sperm motility. To investigate whether fluoride affects the expression of P450, CREM, and ACT, we used immunohistochemical techniques to determine expression levels of these proteins in testes of rats administered 100 mg NaF/L for 2 weeks via drinking water. The results showed that P450 expression was decreased while CREM and ACT expression was increased in the fluoride group, compared to the control. These data suggest that fluoride can impair male reproduction by affecting expression of P450, CREM, and ACT in the testes.
[Mh] Termos MeSH primário: Modulador de Elemento de Resposta do AMP Cíclico/biossíntese
Sistema Enzimático do Citocromo P-450/biossíntese
Fluoretos/farmacologia
Regulação da Expressão Gênica/efeitos dos fármacos
Testículo/metabolismo
Fatores de Transcrição/biossíntese
[Mh] Termos MeSH secundário: Animais
Masculino
Ratos
Ratos Wistar
Motilidade Espermática/efeitos dos fármacos
Espermatogênese/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Crem protein, rat); 0 (Transcription Factors); 0 (activator of CREM in testis (ACT)); 135844-64-3 (Cyclic AMP Response Element Modulator); 9035-51-2 (Cytochrome P-450 Enzyme System); Q80VPU408O (Fluorides)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170119
[Lr] Data última revisão:
170119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160529
[St] Status:MEDLINE
[do] DOI:10.1007/s12011-016-0753-9


  8 / 569 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:28326743
[Au] Autor:Huang Y; Chen CC; Wang TT; Qiu YH; Peng YP
[Ad] Endereço:School of Biological and Basic Medical Sciences, Soochow University, Suzhou, China.
[Ti] Título:Dopamine receptors modulate T lymphocytes via inhibition of cAMP-CREB signaling pathway.
[So] Source:Neuro Endocrinol Lett;37(7):491-500, 2016 Dec.
[Is] ISSN:0172-780X
[Cp] País de publicação:Sweden
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: We have previously reported that dopamine D2-like receptors including D2, D3 and D4 receptors are more important in mediating modulation of T cells than dopamine D1-like receptors (D1 and D5 receptors). Here we aimed to clarify the role of D2-like receptors in regulation of differentiation and function of T lymphocyte subsets, including helper T (Th)1, Th2, Th17 and regulatory T (Treg) cells. METHODS: Lymphocytes, separated from the mesenteric lymph nodes of mice, were stimulated with concanavalin A (Con A) and treated with the D2-like receptor agonist quinpirole or the antagonist haloperidol. Expression of lymphocyte cytokines and transcription factors and dopamine D2, D3 and D4 receptors were measured by real-time quantitative polymerase chain reaction and Western blot assay. Meanwhile, cAMP and phosphorylated cAMP-response element-binding (CREB) levels in the lymphocytes were examined by enzyme-linked immunosorbent assay and Western blot assay, respectively. RESULTS: Activation of D2-like receptors with the agonist quinpirole upregulated the expression of Th2- and Treg-specific transcription factors and cytokines in Con A-activated lymphocytes, but downregulated the expression of Th1- and Th17-specific transcription factors and cytokines. Simultaneously, quinpirole increased dopamine D3 and D4 receptor expression, but did not alter D2 receptor expression. However, quinpirole reduced both cAMP and phosphorylated CREB levels in Con A-activated lymphocytes. All these quinpirole effects were blocked by haloperidol, an antagonist of D2-like receptors. CONCLUSIONS: D2-like receptors, principally dopamine D3 and D4 receptors, promote differentiation and function of T lymphocytes towards anti-inflammatory T cell subsets by a negative link to cAMP-CREB pathway.
[Mh] Termos MeSH primário: Receptores Dopaminérgicos/metabolismo
Transdução de Sinais/efeitos dos fármacos
Linfócitos T/metabolismo
[Mh] Termos MeSH secundário: Animais
AMP Cíclico/metabolismo
Modulador de Elemento de Resposta do AMP Cíclico/metabolismo
Agonistas de Dopamina/farmacologia
Antagonistas de Dopamina/farmacologia
Ensaio de Imunoadsorção Enzimática
Camundongos Endogâmicos ICR
Fosforilação
Quimpirol/farmacologia
Receptores Dopaminérgicos/efeitos dos fármacos
Linfócitos T/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dopamine Agonists); 0 (Dopamine Antagonists); 0 (Receptors, Dopamine); 135844-64-3 (Cyclic AMP Response Element Modulator); 20OP60125T (Quinpirole); E0399OZS9N (Cyclic AMP)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170622
[Lr] Data última revisão:
170622
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170323
[St] Status:MEDLINE


  9 / 569 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27987522
[Au] Autor:Guo Q; Chen XY; Su Y
[Ad] Endereço:Department of Rheumatology and Immunology, Peking University People's Hospital, Beijing 100044, China; Department of Rheumatology and Immunology, Peking University International Hospital, Beijing 102206, China.
[Ti] Título:[Interleukin-2 signaling pathway regulating molecules in systemic lupus erythematosus].
[So] Source:Beijing Da Xue Xue Bao Yi Xue Ban;48(6):1100-1104, 2016 12 18.
[Is] ISSN:1671-167X
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Systemic lupus erythematosus (SLE) is a prototypic systemic autoimmune disease, which characterized by complex immunological abnormalities and multiple tissue and organ damages. The etiology and pathogenesis of SLE have not been entirely recognized. Genetic, environmental and viral infections and other factors might be related to the pathogenetic mechanisms of SLE. Interleukin-2 (IL-2) is a critical cytokine produced by T cells upon activation and is important for the generation of T regulatory cells and activation-induced cell death. In SLE patients, T cells display decreased capacity to produce IL-2. Impaired IL-2 expression resulted in decreased generation of regulatory T lymphocytes, and defect of activation-induced cell death. Former researches indicated that IL-2 deficiency in SLE is important for the pathogenesis and treatment of SLE. Several regulating molecules can affect the transcription of IL-2 gene and had an important role in the pathogenesis of SLE. These molecules include cyclic AMP-responsive element modulator (CREM), protein phosphatase 2A (PP2A), E-74 like factor 1 (Elf-1), B lymphocyte induced maturation protein-1 (Blimp-1) and interferon regulator factor 5 (IRF-5). CREM is a transcriptional inhibitor that can repress the transcription of the IL-2 gene by binding to the promoter of the IL-2 gene. PP2A is a Ser/Thr phosphatase that expressed in eukaryotic cells ubiquitously, it represents a negative regulator of the IL-2 gene promoter activity. Elf-1 belongs to the Ets family of transcription factors and can promote the expression of IL-2. Blimp-1 is a crucial transcription factors for regulating B lymphocyte terminal differentiation, an important function of Blimp-1 in T cells is to repress IL-2 gene transcription directly. Interferon regulatory factors (IRFs) are distinctive transcriptional regulators of type I interferons (IFNs) and IFN inducible genes, IRF-5 is a member of the IRFs family. IRF-5 is found to be increased in SLE and can regulate the production of IL-2 negatively. PP2A can inhibit the synthesis of IL-2 in two ways: on the one hand, activating the IL-2 transcription inhibitory factor CREMα, on the other hand, inhibiting IL-2 stimulating transcription factor Elf-1. While IRF-5 can activate the IL-2 transcription negative regulator Blimp-1 as to inhibit IL-2 expression. These molecules participate in the regulation of IL-2 through different pathways. This paper reviews the current knowledge of IL-2 signaling pathway regulating molecules in SLE.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica/genética
Regulação da Expressão Gênica/imunologia
Interleucina-2/genética
Interleucina-2/imunologia
Lúpus Eritematoso Sistêmico/genética
Lúpus Eritematoso Sistêmico/imunologia
Lúpus Eritematoso Sistêmico/fisiopatologia
[Mh] Termos MeSH secundário: Modulador de Elemento de Resposta do AMP Cíclico/genética
Modulador de Elemento de Resposta do AMP Cíclico/imunologia
Seres Humanos
Fatores Reguladores de Interferon/genética
Fatores Reguladores de Interferon/imunologia
Proteínas Nucleares/genética
Proteínas Nucleares/imunologia
Regiões Promotoras Genéticas/genética
Regiões Promotoras Genéticas/imunologia
Proteína Fosfatase 2/genética
Proteína Fosfatase 2/imunologia
Transdução de Sinais/genética
Transdução de Sinais/imunologia
Linfócitos T Reguladores/imunologia
Fatores de Transcrição/genética
Fatores de Transcrição/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (CREM protein, human); 0 (ELF1 protein, human); 0 (IRF5 protein, human); 0 (Interferon Regulatory Factors); 0 (Interleukin-2); 0 (Nuclear Proteins); 0 (Transcription Factors); 135844-64-3 (Cyclic AMP Response Element Modulator); EC 3.1.3.16 (Protein Phosphatase 2)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161218
[St] Status:MEDLINE


  10 / 569 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
[PMID]:27904655
[Au] Autor:Zhang Q; Ding S; Zhang H; Long H; Wu H; Zhao M; Chan V; Lau CS; Lu Q
[Ad] Endereço:Department of Dermatology, Second Xiangya Hospital, Central South University, Changsha, Hunan 410011 China.
[Ti] Título:Increased Set1 binding at the promoter induces aberrant epigenetic alterations and up-regulates cyclic adenosine 5'-monophosphate response element modulator alpha in systemic lupus erythematosus.
[So] Source:Clin Epigenetics;8:126, 2016.
[Is] ISSN:1868-7083
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Up-regulated cyclic adenosine 5'-monophosphate response element modulator α (CREMα) which can inhibit IL-2 and induce IL-17A in T cells plays a critical role in the pathogenesis of systemic lupus erythematosus (SLE). This research aimed to investigate the mechanisms regulating CREMα expression in SLE. RESULTS: From the chromatin immunoprecipitation (ChIP) microarray data, we found a sharply increased H3 lysine 4 trimethylation (H3K4me3) amount at the CREMα promoter in SLE CD4+ T cells compared to controls. Then, by ChIP and real-time PCR, we confirmed this result. Moreover, H3K4me3 amount at the promoter was positively correlated with CREMα mRNA level in SLE CD4+ T cells. In addition, a striking increase was observed in SET domain containing 1 (Set1) enrichment, but no marked change in mixed-lineage leukemia 1 (MLL1) enrichment at the CREMα promoter in SLE CD4+ T cells. We also proved Set1 enrichment was positively correlated with both H3K4me3 amount at the CREMα promoter and CREMα mRNA level in SLE CD4+ T cells. Knocking down Set1 with siRNA in SLE CD4+ T cells decreased Set1 and H3K4me3 enrichments, and elevated the levels of DNMT3a and DNA methylation, while the amounts of H3 acetylation (H3ac) and H4 acetylation (H4ac) didn't alter greatly at the CREMα promoter. All these changes inhibited the expression of CREMα, then augmented IL-2 and down-modulated IL-17A productions. Subsequently, we observed that DNA methyltransferase (DNMT) 3a enrichment at the CREMα promoter was down-regulated significantly in SLE CD4+ T cells, and H3K4me3 amount was negatively correlated with both DNA methylation level and DNMT3a enrichment at the CREMα promoter in SLE CD4+ T cells. CONCLUSIONS: In SLE CD4+ T cells, increased Set1 enrichment up-regulates H3K4me3 amount at the CREMα promoter, which antagonizes DNMT3a and suppresses DNA methylation within this region. All these factors induce CREMα overexpression, consequently result in IL-2 under-expression and IL-17A overproduction, and contribute to SLE at last. Our findings provide a novel approach in SLE treatment.
[Mh] Termos MeSH primário: Modulador de Elemento de Resposta do AMP Cíclico/genética
Histona-Lisina N-Metiltransferase/metabolismo
Lúpus Eritematoso Sistêmico/genética
Lúpus Eritematoso Sistêmico/metabolismo
Regulação para Cima
[Mh] Termos MeSH secundário: Adulto
Linfócitos T CD4-Positivos/metabolismo
Imunoprecipitação da Cromatina/métodos
Metilação de DNA
Epigênese Genética
Feminino
Histona-Lisina N-Metiltransferase/genética
Histonas/metabolismo
Seres Humanos
Interleucina-17/genética
Interleucina-2/genética
Lúpus Eritematoso Sistêmico/imunologia
Masculino
Análise de Sequência com Séries de Oligonucleotídeos/métodos
Regiões Promotoras Genéticas
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CREM protein, human); 0 (Histones); 0 (IL17A protein, human); 0 (IL2 protein, human); 0 (Interleukin-17); 0 (Interleukin-2); 135844-64-3 (Cyclic AMP Response Element Modulator); EC 2.1.1.43 (Histone-Lysine N-Methyltransferase); EC 2.1.1.43 (Setd1A protein, human)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170428
[Lr] Data última revisão:
170428
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161202
[St] Status:MEDLINE



página 1 de 57 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde