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[PMID]:29381923
[Au] Autor:Yang Y; Chu FH; Xu WR; Sun JQ; Sun X; Ma XM; Yu MW; Yang GW; Wang XM
[Ad] Endereço:Department of Oncology, Beijing Hospital of Traditional Chinese Medicine Affiliated to Capital Medical University.
[Ti] Título:Identification of regulatory role of DNA methylation in colon cancer gene expression via systematic bioinformatics analysis.
[So] Source:Medicine (Baltimore);96(47):e8487, 2017 Nov.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Colon cancer arises from the accumulations of genetic and epigenetic changes. Currently, profiles of DNA methylation and gene expression of colon cancer have not been elucidated clearly. This articles aims to characterize the profile of DNA methylation and gene expression of colon cancer systemically, and acquire candidate genes potentially regulated by altered methylation for this disease.Data were downloaded from The Cancer Genome Atlas database. Differentially methylated CpG sites (DMCs) and differentially methylated regions (DMRs) were calculated via COHCAP. Differentially expressed genes (DEGs) were identified by DESeq2. Weighted gene co-expression network analysis (WGCNA) package in R was applied for WGCNA.Data of 275 solid tumor tissues and 19 adjacent tumor tissues of colon cancer were obtained. A total of 1828 DMCs, including 1390 hypermethylated and 438 hypomethylated CpG sites, were identified between tumor and normal groups. A total of 789 DEGs, containing 435 upregulated genes and 354 downregulated genes were observed. It revealed that 8 DMRs-DEGs and 95 DMCs-DEGs pairs were significantly correlated. Furthermore, genes of yellow and brown modules from WGCNA were significantly correlated with tumor/normal status, and significantly enriched in peroxisome proliferator activated receptor signaling pathway, glutamatergic synapse, and neuroactive ligand-receptor interaction. Genes in the above 2 modules were also significantly enriched in DMCs or DMRs-associated genes. Specifically, ADHFE1, HAND2, and GNAO1 were hypermethylated and downregulated in colon cancer, suggesting that the low expression levels of these genes may be regulated by DNA hypermethylation. In addition, the 3 genes were involved in brown module of WGCNA, indicating their important roles in colon cancer.The investigation of the relationship between DNA methylation and gene expression may help to understand the effect of DNA methylation alteration on genes expression, especially gene co-expression network in the development of colon cancer. Genes such as ADHFE1, HAND2, and GNAO1 may be served as potential candidates for diagnosis and therapy targets in colon cancer.
[Mh] Termos MeSH primário: Neoplasias do Colo/genética
Neoplasias do Colo/fisiopatologia
Metilação de DNA/fisiologia
Expressão Gênica/fisiologia
[Mh] Termos MeSH secundário: Oxirredutases do Álcool/metabolismo
Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo
Ilhas de CpG/fisiologia
Bases de Dados Genéticas
Subunidades alfa Gi-Go de Proteínas de Ligação ao GTP/metabolismo
Redes Reguladoras de Genes/fisiologia
Seres Humanos
Proteínas Mitocondriais/metabolismo
Receptores Ativados por Proliferador de Peroxissomo/metabolismo
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (GNAO1 protein, human); 0 (HAND2 protein, human); 0 (Mitochondrial Proteins); 0 (Peroxisome Proliferator-Activated Receptors); EC 1.1.- (Alcohol Oxidoreductases); EC 1.1.99.24 (hydroxyacid-oxoacid transhydrogenase); EC 3.6.5.1 (GTP-Binding Protein alpha Subunits, Gi-Go)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008487


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[PMID]:28844908
[Au] Autor:Laprairie RB; Denovan-Wright EM; Wright JM
[Ad] Endereço:Department of Pharmacology, Dalhousie University, Halifax, Nova Scotia, Canada. Electronic address: robert.laprairie@dal.ca.
[Ti] Título:Differential regulation of the duplicated fabp7, fabp10 and fabp11 genes of zebrafish by peroxisome proliferator activated receptors.
[So] Source:Comp Biochem Physiol B Biochem Mol Biol;213:81-90, 2017 Nov.
[Is] ISSN:1879-1107
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In the duplication-degeneration-complementation model, duplicated gene-pairs undergo nonfunctionalization (loss from the genome), subfunctionalization (the functions of the ancestral gene are sub-divided between duplicate genes), or neofunctionalization (one of the duplicate genes acquires a new function). These processes occur by loss or gain of regulatory elements in gene promoters. Fatty acid-binding proteins (Fabp) belong to a multigene family composed of orthologous proteins that are highly conserved in sequence and function, but differ in their gene regulation. We previously reported that the zebrafish fabp1a, fabp1b.1, and fabp1b.2 promoters underwent subfunctionalization of PPAR responsiveness. Here, we describe the regulation at the duplicated zebrafish fabp7a/fabp7b, fabp10a/fabp10b and fabp11a/fabp11b gene promoters. Differential control at the duplicated fabp promoters was assessed by DNA sequence analysis, responsiveness to PPAR-isoform specific agonists and NF-κB p50 antagonists in zebrafish liver and intestine explant tissue, and in HEK293A cells transfected with fabp promoter-reporter constructs. Each zebrafish fabp gene displayed unique transcriptional regulation compared to its paralogous duplicate. This work provides a framework to account for the evolutionary trajectories that led to the high retention (57%) of duplicated fabp genes in the zebrafish genome compared to only ~3% of all duplicated genes in the zebrafish genome.
[Mh] Termos MeSH primário: Proteína 7 de Ligação a Ácidos Graxos/biossíntese
Proteínas de Ligação a Ácido Graxo/biossíntese
Duplicação Gênica
Regulação da Expressão Gênica/fisiologia
Receptores Ativados por Proliferador de Peroxissomo/metabolismo
Proteínas de Peixe-Zebra/biossíntese
Peixe-Zebra/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteína 7 de Ligação a Ácidos Graxos/genética
Proteínas de Ligação a Ácido Graxo/genética
Células HEK293
Seres Humanos
Subunidade p50 de NF-kappa B/genética
Subunidade p50 de NF-kappa B/metabolismo
Receptores Ativados por Proliferador de Peroxissomo/genética
Regiões Promotoras Genéticas/fisiologia
Peixe-Zebra/genética
Proteínas de Peixe-Zebra/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fabp11 protein, zebrafish); 0 (Fatty Acid-Binding Protein 7); 0 (Fatty Acid-Binding Proteins); 0 (NF-kappa B p50 Subunit); 0 (NFKB1 protein, human); 0 (Peroxisome Proliferator-Activated Receptors); 0 (Zebrafish Proteins); 0 (fabp7a protein, zebrafish); 0 (fatty acid-binding protein 10, zebrafish)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170829
[St] Status:MEDLINE


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[PMID]:28830207
[Au] Autor:Park J; Bui PTC; Song H; Kim SK; Rhee DK; Kim EY; Rhyu MR; Lee MS; Lee YJ
[Ad] Endereço:* Department of Bioscience and Biotechnology, College of Life Science, Sejong University, Kwangjingu, Kunjadong, Seoul 04310, Republic of Korea.
[Ti] Título:Ginseng on Nuclear Hormone Receptors.
[So] Source:Am J Chin Med;45(6):1147-1156, 2017.
[Is] ISSN:0192-415X
[Cp] País de publicação:Singapore
[La] Idioma:eng
[Ab] Resumo:The first record of ginseng use dates back over two millennia, and ginseng is now popular in more than 35 countries. Ginsenosides are the pharmacological constituents responsible for the beneficial effects of ginseng. There is increasing evidence that ginseng and its bioactive ingredients are involved in the regulation of nuclear receptors, molecules that act in response to the specific binding of hormones, which link to a diverse array of signaling pathways, such as the ERK and PI3K/Akt pathways. Knowledge of the mechanism of how ginseng mediates these complexes is essential for the development of multi-target phytomedicine as possible therapy for different diseases. Here, we discuss the literature on the effects of ginseng and its constituents on estrogen, glucocorticoid, peroxisome proliferator-activated, and androgen nuclear hormone receptors, as well as how ginseng and its constituents exert their biological function in the treatment of cancer, obesity, and cardiovascular and neurological disorders. The accumulated results definitely show that the nuclear receptors are cellular targets of ginsenosides, but more rigorous data are required to establish and provide a scientific basis to confirm the suggested efficacy of ginseng or products with ginsenosides.
[Mh] Termos MeSH primário: Ginsenosídeos/farmacologia
Ginsenosídeos/uso terapêutico
Panax/química
Fitoterapia
Extratos Vegetais/farmacologia
Extratos Vegetais/uso terapêutico
Receptores Citoplasmáticos e Nucleares/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Doenças Cardiovasculares/tratamento farmacológico
Feminino
Ginsenosídeos/isolamento & purificação
Seres Humanos
Sistema de Sinalização das MAP Quinases
Masculino
Neoplasias/tratamento farmacológico
Doenças do Sistema Nervoso/tratamento farmacológico
Obesidade/tratamento farmacológico
Receptores Ativados por Proliferador de Peroxissomo/efeitos dos fármacos
Receptores Ativados por Proliferador de Peroxissomo/fisiologia
Extratos Vegetais/isolamento & purificação
Receptores Androgênicos/efeitos dos fármacos
Receptores Androgênicos/fisiologia
Receptores Citoplasmáticos e Nucleares/fisiologia
Receptores Estrogênicos/efeitos dos fármacos
Receptores Estrogênicos/fisiologia
Receptores de Glucocorticoides/efeitos dos fármacos
Receptores de Glucocorticoides/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Ginsenosides); 0 (Peroxisome Proliferator-Activated Receptors); 0 (Plant Extracts); 0 (Receptors, Androgen); 0 (Receptors, Cytoplasmic and Nuclear); 0 (Receptors, Estrogen); 0 (Receptors, Glucocorticoid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE
[do] DOI:10.1142/S0192415X17500628


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[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


  5 / 1689 MEDLINE  
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[PMID]:28687332
[Au] Autor:Chen L; Zhu Z; Gao W; Jiang Q; Yu J; Fu C
[Ad] Endereço:Department of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China.
[Ti] Título:Systemic analysis of different colorectal cancer cell lines and TCGA datasets identified IGF-1R/EGFR-PPAR-CASPASE axis as important indicator for radiotherapy sensitivity.
[So] Source:Gene;627:484-490, 2017 Sep 05.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Insulin-like growth factor 1 receptor (IGF-1R) is proved to contribute the development of many types of cancers. But, little is known about its roles in radio-resistance of colorectal cancer (CRC). Here, we demonstrated that low IGF-1R expression value was associated with the better radiotherapy sensitivity of CRC. Besides, through Quantitative Real-time PCR (qRT-PCR), the elevated expression value of epidermal growth factor receptor (EGFR) was observed in CRC cell lines (HT29, RKO) with high radio-sensitivity compared with those with low sensitivity (SW480, LOVO). The irradiation induced apoptosis rates of wild type and EGFR agonist (EGF) or IGF-1R inhibitor (NVP-ADW742) treated HT29 and SW480 cells were quantified by flow cytometry. As a result, the apoptosis rate of EGF and NVP-ADW742 treated HT29 cells was significantly higher than that of those wild type ones, which indicated that high EGFR and low IGF-1R expression level in CRC was associated with the high sensitivity to radiotherapy. We next conducted systemic bioinformatics analysis of genome-wide expression profiles of CRC samples from the Cancer Genome Atlas (TCGA). Differential expression analysis between IGF-1R and EGFR abnormal CRC samples, i.e. CRC samples with higher IGF-1R and lower EGFR expression levels based on their median expression values, and the rest of CRC samples identified potential genes contribute to radiotherapy sensitivity. Functional enrichment of analysis of those differential expression genes (DEGs) in the Database for Annotation, Visualization and Integrated Discovery (DAVID) indicated PPAR signaling pathway as an important pathway for the radio-resistance of CRC. Our study identified the potential biomarkers for the rational selection of radiotherapy for CRC patients.
[Mh] Termos MeSH primário: Caspases/genética
Neoplasias Colorretais/metabolismo
Receptores Ativados por Proliferador de Peroxissomo/genética
Tolerância a Radiação/genética
Receptor IGF Tipo 1/genética
[Mh] Termos MeSH secundário: Caspases/metabolismo
Neoplasias Colorretais/genética
Células HT29
Seres Humanos
Receptores Ativados por Proliferador de Peroxissomo/metabolismo
Receptor IGF Tipo 1/antagonistas & inibidores
Receptor IGF Tipo 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Peroxisome Proliferator-Activated Receptors); EC 2.7.10.1 (Receptor, IGF Type 1); EC 3.4.22.- (Caspases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170709
[St] Status:MEDLINE


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[PMID]:28665967
[Au] Autor:Ji W; Zhao M; Wang M; Yan W; Liu Y; Ren S; Lu J; Wang B; Chen L
[Ad] Endereço:Department of Pharmacology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China.
[Ti] Título:Effects of canagliflozin on weight loss in high-fat diet-induced obese mice.
[So] Source:PLoS One;12(6):e0179960, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Canagliflozin, an inhibitor of sodium glucose co-transporter (SGLT) 2, has been shown to reduce body weight during the treatment of type 2 diabetes mellitus (T2DM). In this study, we sought to determine the role of canagliflozin in body weight loss and liver injury in obesity. C57BL/6J mice were fed a high-fat diet to simulate diet-induced obesity (DIO). Canagliflozin (15 and 60 mg/kg) was administered to DIO mice for 4 weeks. Orlistat (10 mg/kg) was used as a positive control. The body weight, liver weight, liver morphology, total cholesterol (TC) and triglyceride (TG) levels were examined. Signaling molecules, including diacylgycero1 acyltransferase-2 (DGAT2), peroxisome proliferation receptor alpha-1 (PPARα1), PPARγ1, PPARγ2 mRNA levels and the protein expression of SGLT2 were evaluated. Canagliflozin reduced body weight, especially the high-dose canagliflozin, and resulted in increased body weight loss compared with orlistat. Moreover, canagliflozin reduced the liver weight and the ratio of liver weight to body weight, lowered the serum levels of TC and TG, and ameliorated liver steatosis. During the canagliflozin treatment, SGLT2, DGAT2, PPARγ1 and PPARγ2 were inhibited, and PPARα1 was elevated in the liver tissues. This finding may explain why body weight was reduced and secondary liver injury was ameliorated in response to canagliflozin. Together, the results suggest that canagliflozin may be a potential anti-obesity strategy.
[Mh] Termos MeSH primário: Canagliflozina/farmacologia
Dieta Hiperlipídica
Hipoglicemiantes/uso terapêutico
Obesidade/terapia
Perda de Peso/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Colesterol/sangue
Diacilglicerol O-Aciltransferase/metabolismo
Fígado/efeitos dos fármacos
Fígado/patologia
Camundongos
Camundongos Endogâmicos C57BL
Obesidade/enzimologia
Obesidade/etiologia
Obesidade/metabolismo
Receptores Ativados por Proliferador de Peroxissomo/metabolismo
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hypoglycemic Agents); 0 (Peroxisome Proliferator-Activated Receptors); 0 (Triglycerides); 0SAC974Z85 (Canagliflozin); 97C5T2UQ7J (Cholesterol); EC 2.3.1.20 (DGAT2 protein, mouse); EC 2.3.1.20 (Diacylglycerol O-Acyltransferase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170701
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179960


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[PMID]:28426724
[Au] Autor:Vogeler S; Galloway TS; Isupov M; Bean TP
[Ad] Endereço:School of Biosciences, College of Life and Environmental Sciences, University of Exeter, Exeter, United Kingdom.
[Ti] Título:Cloning retinoid and peroxisome proliferator-activated nuclear receptors of the Pacific oyster and in silico binding to environmental chemicals.
[So] Source:PLoS One;12(4):e0176024, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Disruption of nuclear receptors, a transcription factor superfamily regulating gene expression in animals, is one proposed mechanism through which pollution causes effects in aquatic invertebrates. Environmental pollutants have the ability to interfere with the receptor's functions through direct binding and inducing incorrect signals. Limited knowledge of invertebrate endocrinology and molecular regulatory mechanisms, however, impede the understanding of endocrine disruptive effects in many aquatic invertebrate species. Here, we isolated three nuclear receptors of the Pacific oyster, Crassostrea gigas: two isoforms of the retinoid X receptor, CgRXR-1 and CgRXR-2, a retinoic acid receptor ortholog CgRAR, and a peroxisome proliferator-activated receptor ortholog CgPPAR. Computer modelling of the receptors based on 3D crystal structures of human proteins was used to predict each receptor's ability to bind to different ligands in silico. CgRXR showed high potential to bind and be activated by 9-cis retinoic acid and the organotin tributyltin (TBT). Computer modelling of CgRAR revealed six residues in the ligand binding domain, which prevent the successful interaction with natural and synthetic retinoid ligands. This supports an existing theory of loss of retinoid binding in molluscan RARs. Modelling of CgPPAR was less reliable due to high discrepancies in sequence to its human ortholog. Yet, there are suggestions of binding to TBT, but not to rosiglitazone. The effect of potential receptor ligands on early oyster development was assessed after 24h of chemical exposure. TBT oxide (0.2µg/l), all-trans retinoic acid (ATRA) (0.06 mg/L) and perfluorooctanoic acid (20 mg/L) showed high effects on development (>74% abnormal developed D-shelled larvae), while rosiglitazone (40 mg/L) showed no effect. The results are discussed in relation to a putative direct (TBT) disruption effect on nuclear receptors. The inability of direct binding of ATRA to CgRAR suggests either a disruptive effect through a pathway excluding nuclear receptors or an indirect interaction. Our findings provide valuable information on potential mechanisms of molluscan nuclear receptors and the effects of environmental pollution on aquatic invertebrates.
[Mh] Termos MeSH primário: Poluentes Ambientais/metabolismo
Ostreidae
Receptores Ativados por Proliferador de Peroxissomo/genética
Receptores do Ácido Retinoico/genética
[Mh] Termos MeSH secundário: Animais
Clonagem Molecular
Simulação por Computador
Cristalografia por Raios X
Feminino
Masculino
Ostreidae/embriologia
Receptores Ativados por Proliferador de Peroxissomo/química
Receptores Ativados por Proliferador de Peroxissomo/metabolismo
Conformação Proteica
Receptores do Ácido Retinoico/química
Receptores do Ácido Retinoico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Environmental Pollutants); 0 (Peroxisome Proliferator-Activated Receptors); 0 (Receptors, Retinoic Acid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170421
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0176024


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[PMID]:28424262
[Au] Autor:Wei CC; Wu K; Gao Y; Zhang LH; Li DD; Luo Z
[Ad] Endereço:Key Laboratory of Freshwater Animal Breeding, Ministry of Agriculture, Fishery College, Huazhong Agricultural University, Wuhan, China; and Freshwater Aquaculture Collaborative Innovative Centre of Hubei Province, Wuhan, China.
[Ti] Título:Magnesium Reduces Hepatic Lipid Accumulation in Yellow Catfish ( ) and Modulates Lipogenesis and Lipolysis via PPARA, JAK-STAT, and AMPK Pathways in Hepatocytes.
[So] Source:J Nutr;147(6):1070-1078, 2017 Jun.
[Is] ISSN:1541-6100
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Magnesium influences hepatic lipid deposition in vertebrates, but the underlying mechanism is unknown. We used yellow catfish and their isolated hepatocytes to test the hypothesis that magnesium influences lipid deposition by modulating lipogenesis and lipolysis. Juvenile yellow catfish (mean ± SEM weight: 3.43 ± 0.02 g, 3 mo old, mixed sex) were fed a 0.14- (low), 0.87- (intermediate) or 2.11- (high) g Mg/kg diet for 56 d. Primary hepatocytes were incubated for 48 h in control or MgSO -containing medium with or without 2-h pretreatment with an inhibitor (AG490, GW6471, or Compound C). Growth performance, cell viability, triglyceride (TG) concentrations, and expression of enzymes and genes involved in lipid metabolism were measured. Compared with fish fed low magnesium, those fed intermediate or high magnesium had lower hepatic lipids (18%, 22%) and 6-phosphogluconate dehydrogenase (6PGD; 3.7%, 3.8%) and malic enzyme (ME; 35%, 48%) activities and greater mRNA levels of the lipolytic genes adipose triacylglyceride lipase ( ; 82% and 1.7-fold) and peroxisome proliferator-activated receptor ( ; 18% and 1.0-fold), respectively ( < 0.05). Relative mRNA levels of AMP-activated protein kinase ( ) , , , , , , Janus kinase , and signal transducers and activators of transcription ( ) in fish fed high magnesium were higher (24% to 3.1-fold, < 0.05) than in those fed low or intermediate magnesium. Compared with cells incubated with MgSO alone, those incubated with MgSO and pretreated with AG490, GW6471, or Compound C had greater TG concentrations (42%, 31%, or 56%), (98%, 59%, or 51%), (68%, 73%, or 32%) mRNA expression, and activities of G6PD (35%, 45%, or 16%) and ME (1.5-fold, 1.3-fold, or 13%), and reduced upregulation (61%, 25%, or 45%) of the lipolytic gene, ( < 0.05). Magnesium reduced hepatic lipid accumulation in yellow catfish and the variation might be attributed to inhibited lipogenesis and increased lipolysis. PPARA, JAK-STAT, and AMPK pathways mediated the magnesium-induced changes in lipid deposition and metabolism. These results offer new insight into magnesium nutrition in vertebrates.
[Mh] Termos MeSH primário: Fenômenos Fisiológicos da Nutrição Animal
Peixes-Gato/metabolismo
Dieta
Metabolismo dos Lipídeos/efeitos dos fármacos
Fígado/efeitos dos fármacos
Magnésio/farmacologia
Oligoelementos/farmacologia
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/metabolismo
Ração Animal
Animais
Aquicultura
Feminino
Hepatócitos/efeitos dos fármacos
Hepatócitos/metabolismo
Janus Quinases/metabolismo
Lipídeos
Lipogênese/efeitos dos fármacos
Lipólise/efeitos dos fármacos
Fígado/citologia
Fígado/metabolismo
Masculino
Receptores Ativados por Proliferador de Peroxissomo/metabolismo
RNA Mensageiro/metabolismo
Fatores de Transcrição STAT/metabolismo
Triglicerídeos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipids); 0 (Peroxisome Proliferator-Activated Receptors); 0 (RNA, Messenger); 0 (STAT Transcription Factors); 0 (Trace Elements); 0 (Triglycerides); EC 2.7.10.2 (Janus Kinases); EC 2.7.11.31 (AMP-Activated Protein Kinases); I38ZP9992A (Magnesium)
[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:170421
[St] Status:MEDLINE
[do] DOI:10.3945/jn.116.245852


  9 / 1689 MEDLINE  
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[PMID]:28414176
[Au] Autor:Madureira TV; Pinheiro I; de Paula Freire R; Rocha E; Castro LF; Urbatzka R
[Ad] Endereço:CIIMAR - Interdisciplinary Centre for Marine and Environmental Research, University of Porto (U.Porto), Terminal de Cruzeiros do Porto de Leixões, Av. General Norton de Matos s/n, 4450-208 Matosinhos, Portugal; ICBAS - Institute of Biomedical Sciences Abel Salazar, Department of Microscopy, Laborato
[Ti] Título:Genome specific PPARαB duplicates in salmonids and insights into estrogenic regulation in brown trout.
[So] Source:Comp Biochem Physiol B Biochem Mol Biol;208-209:94-101, 2017 Jun.
[Is] ISSN:1879-1107
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Peroxisome proliferator-activated receptors (PPARs) are key regulators of many processes in vertebrates, such as carbohydrate and lipid metabolism. PPARα, a member of the PPAR nuclear receptor gene subfamily (NR1C1), is involved in fatty acid metabolism, namely in peroxisomal ß-oxidation. Two gene paralogues, pparαA and pparαB, were described in several teleost species with their origin dating back to the teleost-specific genome duplication (3R). Given the additional salmonid-specific genome duplication (4R), four genes could be theoretically anticipated for this gene subfamily. In this work, we examined the pparα gene repertoire in brown trout, Salmo trutta f. fario. Data disclosed two pparα-like sequences in brown trout. Phylogenetic analyses further revealed that the isolated genes are most likely genome pparαB duplicates, pparαBa and pparαBb, while pparαA is apparently absent in salmonids. Both genes showed a ubiquitous mRNA expression across a panel of 11 different organs. In vitro exposed primary brown trout hepatocytes strongly suggest that pparα gene paralogues are differently regulated by ethinylestradiol (EE2). PparαBb mRNA expression significantly decreased with dosage, reaching significance after exposure to 50µM EE2, while pparαBa mRNA increased, significant at 1µM EE2. The present data enhances the understanding of pparα function and evolution in teleost, and reinforces the evidence of a potential crosstalk between estrogenic and pparα signaling pathways.
[Mh] Termos MeSH primário: Estrogênios/farmacologia
Regulação da Expressão Gênica/efeitos dos fármacos
Genoma
Hepatócitos/metabolismo
Receptores Ativados por Proliferador de Peroxissomo/genética
Truta/genética
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Hepatócitos/citologia
Hepatócitos/efeitos dos fármacos
Filogenia
Reação em Cadeia da Polimerase em Tempo Real
Truta/crescimento & desenvolvimento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogens); 0 (Peroxisome Proliferator-Activated Receptors)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170623
[Lr] Data última revisão:
170623
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170418
[St] Status:MEDLINE


  10 / 1689 MEDLINE  
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[PMID]:28412042
[Au] Autor:Pluchart H; Khouri C; Blaise S; Roustit M; Cracowski JL
[Ad] Endereço:Unité de Pharmacologie Clinique, Institut National de la Santé et de la Recherche Médicale (INSERM) Centre d'Investigation Clinique (CIC) 1406, Centre Hospitalier Universitaire (CHU) Grenoble-Alpes, 38000 Grenoble, France.
[Ti] Título:Targeting the Prostacyclin Pathway: Beyond Pulmonary Arterial Hypertension.
[So] Source:Trends Pharmacol Sci;38(6):512-523, 2017 Jun.
[Is] ISSN:1873-3735
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Pioneering work demonstrated that an unstable substance isolated from rabbit and pig aortas could relax arterial smooth muscle and inhibit platelet aggregation. Since then, prostacyclin (prostaglandin I2, PGI ) and its analogs have raised much pharmacological interest. In this review we detail how the PGI signaling pathway is much more complex than was initially anticipated, involving peroxisome proliferator-activated receptors (PPARs), prostaglandin transporters (PGTs), and PGI -thromboxane A (TXA ) receptor (IP TP) heterodimerization. We discuss the distinct affinities of PGI analogs for prostanoid receptors. In addition, we introduce the new direct and indirect pharmacological approaches to targeting the PGI pathway within the systemic circulation, including non-prostanoid agonists of the prostacyclin receptor (IP) and PGT inhibitors, as well as transcutaneous pathways using iontophoresis and nanostructured lipid carriers.
[Mh] Termos MeSH primário: Epoprostenol/metabolismo
Epoprostenol/farmacologia
Hipertensão Pulmonar/tratamento farmacológico
Hipertensão Pulmonar/metabolismo
[Mh] Termos MeSH secundário: Animais
Sistema Cardiovascular/efeitos dos fármacos
Sistema Cardiovascular/metabolismo
Epoprostenol/agonistas
Epoprostenol/análogos & derivados
Seres Humanos
Receptores Ativados por Proliferador de Peroxissomo/metabolismo
Receptores de Prostaglandina/agonistas
Receptores de Prostaglandina/metabolismo
Transdução de Sinais/efeitos dos fármacos
Vasoconstrição/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Peroxisome Proliferator-Activated Receptors); 0 (Receptors, Prostaglandin); DCR9Z582X0 (Epoprostenol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170417
[St] Status:MEDLINE



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