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Pesquisa : D12.776.624.664.700.830.500 [Categoria DeCS]
Referências encontradas : 463 [refinar]
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[PMID]:28911146
[Au] Autor:van Gucht ALM; Meima ME; Moran C; Agostini M; Tylki-Szymanska A; Krajewska MW; Chrzanowska K; Efthymiadou A; Chrysis D; Demir K; Visser WE; Visser TJ; Chatterjee K; van Dijk TB; Peeters RP
[Ad] Endereço:Department of Internal Medicine, Erasmus University Medical Center, 3000 Rotterdam, The Netherlands.
[Ti] Título:Anemia in Patients With Resistance to Thyroid Hormone α: A Role for Thyroid Hormone Receptor α in Human Erythropoiesis.
[So] Source:J Clin Endocrinol Metab;102(9):3517-3525, 2017 Sep 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: Patients with resistance to thyroid hormone (TH) α (RTHα) are characterized by growth retardation, macrocephaly, constipation, and abnormal thyroid function tests. In addition, almost all RTHα patients have mild anemia, the pathogenesis of which is unknown. Animal studies suggest an important role for TH and TH receptor (TR)α in erythropoiesis. Objective: To investigate whether a defect in TRα affects the maturation of red blood cells in RTHα patients. Design, Setting, and Patients: Cultures of primary human erythroid progenitor cells (HEPs), from peripheral blood of RTHα patients (n = 11) harboring different inactivating mutations in TRα (P398R, F397fs406X, C392X, R384H, A382fs388X, A263V, A263S), were compared with healthy controls (n = 11). During differentiation, erythroid cells become smaller, accumulate hemoglobin, and express different cell surface markers. We assessed cell number and cell size, and used cell staining and fluorescence-activated cell sorter analysis to monitor maturation at different time points. Results: After ∼14 days of ex vivo expansion, both control and patient-derived progenitors differentiated spontaneously. However, RTHα-derived cells differentiated more slowly. During spontaneous differentiation, RTHα-derived HEPs were larger, more positive for c-Kit (a proliferation marker), and less positive for glycophorin A (a differentiation marker). The degree of abnormal spontaneous maturation of RTHα-derived progenitors did not correlate with severity of underlying TRα defect. Both control and RTHα-derived progenitors responded similarly when differentiation was induced. T3 exposure accelerated differentiation of both control- and RTHα patient-derived HEPs. Conclusions: Inactivating mutations in human TRα affect the balance between proliferation and differentiation of progenitor cells during erythropoiesis, which may contribute to the mild anemia seen in most RTHα patients.
[Mh] Termos MeSH primário: Anemia/genética
Eritropoese/genética
Regulação da Expressão Gênica
Receptores alfa dos Hormônios Tireóideos/genética
Síndrome da Resistência aos Hormônios Tireóideos/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Anemia/epidemiologia
Anemia/fisiopatologia
Estudos de Casos e Controles
Células Cultivadas
Criança
Pré-Escolar
Eritrócitos/metabolismo
Feminino
Seres Humanos
Incidência
Masculino
Meia-Idade
Mutação
Prognóstico
Valores de Referência
Papel (Figurativo)
Células-Tronco/citologia
Células-Tronco/fisiologia
Síndrome da Resistência aos Hormônios Tireóideos/epidemiologia
Síndrome da Resistência aos Hormônios Tireóideos/fisiopatologia
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Thyroid Hormone Receptors alpha)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2017-00840


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[PMID]:28910278
[Au] Autor:Park S; Han CR; Park JW; Zhao L; Zhu X; Willingham M; Bodine DM; Cheng SY
[Ad] Endereço:Laboratory of Molecular Biology, the Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, United States of America.
[Ti] Título:Defective erythropoiesis caused by mutations of the thyroid hormone receptor α gene.
[So] Source:PLoS Genet;13(9):e1006991, 2017 Sep.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Patients with mutations of the THRA gene exhibit classical features of hypothyroidism, including erythroid disorders. We previously created a mutant mouse expressing a mutated TRα1 (denoted as PV; Thra1PV/+ mouse) that faithfully reproduces the classical hypothyroidism seen in patients. Using Thra1PV/+ mice, we explored how the TRα1PV mutant acted to cause abnormalities in erythropoiesis. Thra1PV/+ mice exhibited abnormal red blood cell indices similarly as reported for patients. The total bone marrow cells and erythrocytic progenitors were markedly reduced in the bone marrow of Thra1PV/+ mice. In vitro terminal differentiation assays showed a significant reduction of mature erythrocytes in Thra1PV/+ mice. In wild-type mice, the clonogenic potential of progenitors in the erythrocytic lineage was stimulated by thyroid hormone (T3), suggesting that T3 could directly accelerate the differentiation of progenitors to mature erythrocytes. Analysis of gene expression profiles showed that the key regulator of erythropoiesis, the Gata-1 gene, and its regulated genes, such as the Klf1, ß-globin, dematin genes, CAII, band3 and eALAS genes, involved in the maturation of erythrocytes, was decreased in the bone marrow cells of Thra1PV/+ mice. We further elucidated that the Gata-1 gene was a T3-directly regulated gene and that TRα1PV could impair erythropoiesis via repression of the Gata-1 gene and its regulated genes. These results provide new insights into how TRα1 mutants acted to cause erythroid abnormalities in patients with mutations of the THRA gene. Importantly, the Thra1PV/+ mouse could serve as a preclinical mouse model to identify novel molecular targets for treatment of erythroid disorders.
[Mh] Termos MeSH primário: Eritropoese/genética
Fator de Transcrição GATA1/genética
Hipotireoidismo/genética
Receptores alfa dos Hormônios Tireóideos/genética
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/genética
Eritrócitos
Seres Humanos
Hipotireoidismo/fisiopatologia
Fatores de Transcrição Kruppel-Like/genética
Camundongos
Camundongos Transgênicos
Mutação
Transcriptoma
Tri-Iodotironina/genética
Globinas beta/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GATA1 Transcription Factor); 0 (Gata1 protein, mouse); 0 (Kruppel-Like Transcription Factors); 0 (Thyroid Hormone Receptors alpha); 0 (beta-Globins); 0 (erythroid Kruppel-like factor); 06LU7C9H1V (Triiodothyronine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006991


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[PMID]:28794003
[Au] Autor:Sofronova SI; Gaynullina DK; Shvetsova AA; Borzykh AA; Selivanova EK; Kostyunina DS; Sharova AP; Martyanov AA; Tarasova OS
[Ad] Endereço:Institute for Biomedical ProblemsRussian Academy of Sciences, Moscow, Russia sofronova.mailbox@gmail.com.
[Ti] Título:Antenatal/early postnatal hypothyroidism alters arterial tone regulation in 2-week-old rats.
[So] Source:J Endocrinol;235(2):137-151, 2017 Nov.
[Is] ISSN:1479-6805
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The mechanisms of vascular alterations resulting from early thyroid hormones deficiency are poorly understood. We tested the hypothesis that antenatal/early postnatal hypothyroidism would alter the activity of endothelial NO pathway and Rho-kinase pathway, which are specific for developing vasculature. Dams were treated with propylthiouracil (PTU, 7 ppm) in drinking water during gestation and 2 weeks after delivery, and their progeny had normal body weight but markedly reduced blood levels of thyroid hormones (ELISA). Small arteries from 2-week-old male pups were studied using wire myography, qPCR and Western blotting. Mesenteric arteries of PTU pups, compared to controls, demonstrated smaller maximum response to α -adrenergic agonist methoxamine and reduced mRNA contents of smooth muscle differentiation markers α-actin and SERCA2A. Inhibition of basal NO synthesis by l-NNA led to tonic contraction of mesenteric arteries and augmented their contractile responses to methoxamine; both l-NNA effects were impaired in PTU pups. PTU pups demonstrated lower blood level of NO metabolites compared to control group (Griess reaction). Rho-kinase inhibitor Y27632 strongly reduced mesenteric arteries responses to methoxamine in PTU pups, that was accompanied by elevated Rho-kinase content in their arteries in comparison to control ones. Unlike mesenteric, saphenous arteries of PTU pups, compared to controls, had no changes in α-actin and SERCA2A contents and in responses to l-NNA and Y27632. In conclusion, thyroid hormones deficiency suppresses the anticontractile effect of NO and potentiates the procontractile Rho-kinase effects in mesenteric arteries of 2-week-old pups. Such alterations disturb perinatal cardiovascular homeostasis and might lead to cardiovascular pathologies in adulthood.
[Mh] Termos MeSH primário: Hipotireoidismo/induzido quimicamente
Efeitos Tardios da Exposição Pré-Natal
Resistência Vascular/fisiologia
[Mh] Termos MeSH secundário: Animais
Glicemia
Feminino
Regulação da Expressão Gênica
Hipotireoidismo/metabolismo
Iodeto Peroxidase/genética
Iodeto Peroxidase/metabolismo
Gravidez
Propiltiouracila/toxicidade
RNA Mensageiro
Distribuição Aleatória
Ratos
Receptores alfa dos Hormônios Tireóideos/genética
Receptores alfa dos Hormônios Tireóideos/metabolismo
Hormônios Tireóideos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (RNA, Messenger); 0 (Thyroid Hormone Receptors alpha); 0 (Thyroid Hormones); 721M9407IY (Propylthiouracil); EC 1.11.1.- (iodothyronine deiodinase type II); EC 1.11.1.8 (Iodide Peroxidase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.1530/JOE-17-0225


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[PMID]:28583788
[Au] Autor:Charalampoudis P; Agrogiannis G; Kontzoglou K; Kouraklis G; Sotiropoulos GC
[Ad] Endereço:Breast Unit, Second Propedeutic Department of Surgery, Laiko Hospital, Athens University School of Medicine, Athens, Greece; Breast Unit, Guy's and Saint Thomas' NHS Foundation Trust, London, United Kingdom; Division of Cancer Studies, King's College London, United Kingdom. Electronic address: petro
[Ti] Título:Thyroid hormone receptor alpha (TRa) tissue expression in ductal invasive breast cancer: A study combining quantitative immunohistochemistry with digital slide image analysis.
[So] Source:Eur J Surg Oncol;43(8):1428-1432, 2017 Aug.
[Is] ISSN:1532-2157
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In breast cancer, hormonal receptors hold promise for developing novel targeted therapies. The thyroid exerts its actions via the thyroid hormone receptors alpha and beta. The clinical significance of the expression of thyroid hormone receptors in breast cancer is unclear. MATERIAL AND METHODS: We studied thyroid hormone receptor alpha (TRa) expression in 82 samples from 41 women with ductal invasive breast cancer and no thyroid disease. We performed quantitative immunohistochemistry with digital image analysis and correlated TRa expression with clinicopathological parameters. RESULTS: TRa was expressed in both normal breast epithelium and breast cancer, but expression in breast cancer was significantly lower. TRa was expressed significantly less in larger and grade III tumors. Conversely, breast cancers with lymphovascular invasion showed increased TRa expression compared to cancers without lymphovascular invasion. TRa expression was not significantly different between node-positive and node-negative breast cancers, or among different hormonal profiles and intrinsic subtypes. DISCUSSION: This is the first-in-human study to combine quantitative immunohistochemistry with image analysis to study TRa expression in women with ductal invasive breast cancer and no clinical or biochemical evidence of thyroid dysfunction. We confirm that TRa is expressed in both normal and malignant breast epithelium and suggest that TRa expression is downregulated during breast carcinogenesis. Larger and higher grade breast cancers demonstrate partial loss in TRa expression. Alterations in TRa expression take place even in the absence of clinical or biochemical thyroid disease. The underlying mechanism of these findings and their potential significance in survival and relapse mandate further research.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Carcinoma Ductal de Mama/metabolismo
Receptores alfa dos Hormônios Tireóideos/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Neoplasias da Mama/patologia
Carcinoma Ductal de Mama/patologia
Feminino
Seres Humanos
Interpretação de Imagem Assistida por Computador
Imuno-Histoquímica
Excisão de Linfonodo
Metástase Linfática
Meia-Idade
Gradação de Tumores
Invasividade Neoplásica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Thyroid Hormone Receptors alpha)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170607
[St] Status:MEDLINE


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[PMID]:28324024
[Au] Autor:Wen L; Shibata Y; Su D; Fu L; Luu N; Shi YB
[Ad] Endereço:Section on Molecular Morphogenesis, Program on Cell Regulation and Metabolism, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892.
[Ti] Título:Thyroid Hormone Receptor α Controls Developmental Timing and Regulates the Rate and Coordination of Tissue-Specific Metamorphosis in Xenopus tropicalis.
[So] Source:Endocrinology;158(6):1985-1998, 2017 Jun 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thyroid hormone (T3) receptors (TRs) mediate the effects of T3 on organ metabolism and animal development. There are two TR genes, TRα and TRß, in all vertebrates. During animal development, TRα expression is activated earlier than zygotic T3 synthesis and secretion into the plasma, implicating a developmental role of TRα both in the presence and absence of T3. Using T3-dependent amphibian metamorphosis as a model, we previously proposed a dual-function model for TRs, in particular TRα, during development. That is, unliganded TR represses the expression of T3-inducible genes during premetamorphosis to ensure proper animal growth and prevent premature metamorphosis, whereas during metamorphosis, liganded TR activates target gene transcription to promote the transformation of the tadpole into a frog. To determine if TRα has such a dual function, we generated homozygous TRα-knockout animal lines. We show that, indeed, TRα knockout affects both premetamorphic animal development and metamorphosis. Surprisingly, we observed that TRα is not essential for amphibian metamorphosis, given that homozygous knockout animals complete metamorphosis within a similar time period after fertilization as their wild-type siblings. On the other hand, the timing of metamorphosis for different organs is altered by the knockout; limb metamorphosis occurs earlier, whereas intestinal metamorphosis is completed later than in wild-type siblings. Thus, our studies have demonstrated a critical role of endogenous TRα, not only in regulating both the timing and rate of metamorphosis, but also in coordinating temporal metamorphosis of different organs.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica no Desenvolvimento
Metamorfose Biológica/genética
Organogênese/genética
Receptores alfa dos Hormônios Tireóideos/fisiologia
Xenopus/crescimento & desenvolvimento
Xenopus/genética
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Embrião não Mamífero
Feminino
Larva
Masculino
Especificidade de Órgãos/genética
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Thyroid Hormone Receptors alpha)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE
[do] DOI:10.1210/en.2016-1953


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[PMID]:28323943
[Au] Autor:Choi J; Ishizuya-Oka A; Buchholz DR
[Ad] Endereço:Department of Biological Sciences, University of Cincinnati, Cincinnati, Ohio 45221.
[Ti] Título:Growth, Development, and Intestinal Remodeling Occurs in the Absence of Thyroid Hormone Receptor α in Tadpoles of Xenopus tropicalis.
[So] Source:Endocrinology;158(6):1623-1633, 2017 Jun 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During development in all vertebrates, thyroid hormone receptors (TRs) are expressed before as well as during and after the peak in plasma thyroid hormone (TH) levels. Previously, we established a role for unliganded TRα in gene repression and developmental timing using tadpoles of TRα knockout (TRαKO) frogs. Here, we examined the role of liganded TRα on growth, development, and intestinal remodeling during natural and TH-induced metamorphosis. Disrupted TRα had little effect on growth during the larval period, but after metamorphosis, TRαKO juveniles grew more slowly than wild-type (WT) juveniles. TRαKO tadpoles developed faster throughout premetamorphosis when TH was low or absent, and despite their decreased responsivity to exogenous TH, TRαKO tadpoles not only were able to complete TH-dependent metamorphosis but also did so earlier than WT tadpoles. In contrast to external morphology, larval epithelial cell apoptosis and adult cell proliferation of intestinal remodeling were delayed in TRαKO tadpoles. Also, TRαKO intestines did not shrink in length to the full extent, and fewer intestinal folds into the lumen were present in TRαKO compared with WT juveniles. Such delayed remodeling occurred despite higher premetamorphic expression levels of TH target genes important for metamorphic progression-namely, TRß, Klf9, and ST3. Furthermore, the decreased TH-dependent intestinal shrinkage was consistent with reduced TH response gene expression during natural and TH-induced metamorphosis. As in the TRα null mouse model, TRαKO frogs had statistically significant but surprisingly mild growth and development phenotypes with normal survival and fertility.
[Mh] Termos MeSH primário: Intestinos/crescimento & desenvolvimento
Intestinos/fisiologia
Receptores alfa dos Hormônios Tireóideos/genética
Xenopus/crescimento & desenvolvimento
Xenopus/genética
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Fertilidade/genética
Regulação da Expressão Gênica no Desenvolvimento
Técnicas de Inativação de Genes
Larva/genética
Larva/crescimento & desenvolvimento
Metamorfose Biológica/genética
Fenótipo
Xenopus/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Thyroid Hormone Receptors alpha)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE
[do] DOI:10.1210/en.2016-1955


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[PMID]:28007906
[Au] Autor:de Souza JS; Carromeu C; Torres LB; Araujo BH; Cugola FR; Maciel RM; Muotri AR; Giannocco G
[Ad] Endereço:Department of Medicine, Laboratory of Endocrinology and Translational Medicine, Universidade Federal de São Paulo, UNIFESP/EPM, São Paulo, SP, Brazil.
[Ti] Título:IGF1 neuronal response in the absence of MECP2 is dependent on TRalpha 3.
[So] Source:Hum Mol Genet;26(2):270-281, 2017 Jan 15.
[Is] ISSN:1460-2083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Rett syndrome (RTT) is an X-linked neurodevelopmental disorder in which the MECP2 (methyl CpG-binding protein 2) gene is mutated. Recent studies showed that RTT-derived neurons have many cellular deficits when compared to control, such as: less synapses, lower dendritic arborization and reduced spine density. Interestingly, treatment of RTT-derived neurons with Insulin-like Growth Factor 1 (IGF1) could rescue some of these cellular phenotypes. Given the critical role of IGF1 during neurodevelopment, the present study used human induced pluripotent stem cells (iPSCs) from RTT and control individuals to investigate the gene expression profile of IGF1 and IGF1R on different developmental stages of differentiation. We found that the thyroid hormone receptor (TRalpha 3) has a differential expression profile. Thyroid hormone is critical for normal brain development. Our results showed that there is a possible link between IGF1/IGF1R and the TRalpha 3 and that over expression of IGF1R in RTT cells may be the cause of neurites improvement in neural RTT-derived neurons.
[Mh] Termos MeSH primário: Fator de Crescimento Insulin-Like I/genética
Proteína 2 de Ligação a Metil-CpG/genética
Receptores de Somatomedina/genética
Síndrome de Rett/genética
Receptores alfa dos Hormônios Tireóideos/genética
[Mh] Termos MeSH secundário: Diferenciação Celular/genética
Corpos Embrioides/metabolismo
Seres Humanos
Células-Tronco Pluripotentes Induzidas/metabolismo
Células-Tronco Pluripotentes Induzidas/patologia
Transtornos do Neurodesenvolvimento
Plasticidade Neuronal/genética
Neurônios/metabolismo
Neurônios/patologia
Síndrome de Rett/metabolismo
Síndrome de Rett/fisiopatologia
Coluna Vertebral/crescimento & desenvolvimento
Coluna Vertebral/patologia
Sinapses/genética
Sinapses/patologia
Transcriptoma/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IGF1 protein, human); 0 (IGF1R protein, human); 0 (MECP2 protein, human); 0 (Methyl-CpG-Binding Protein 2); 0 (Receptors, Somatomedin); 0 (Thyroid Hormone Receptors alpha); 0 (thyroid hormone receptor alpha, human); 67763-96-6 (Insulin-Like Growth Factor I)
[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:161224
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddw384


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[PMID]:27736670
[Au] Autor:Gong Y; Tian H; Zhang X; Dong Y; Wang W; Ru S
[Ad] Endereço:Marine Life Science College, Ocean University of China, Qingdao, 266003, China.
[Ti] Título:Refuse leachate exposure causes changes of thyroid hormone level and related gene expression in female goldfish (Carassius auratus).
[So] Source:Environ Toxicol Pharmacol;48:46-52, 2016 Dec.
[Is] ISSN:1872-7077
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:To elucidate the potential thyroid disrupting effects of refuse leachate on females, female goldfish (Carassius auratus) were exposed to 0.5% diluted leachates from each step of a leachate treatment process (i.e. raw leachate before treatment, after membrane bioreactor treatment, and the final treated leachate) for 21days. Raw leachate exposure caused disturbances in the thyroid cascade of female fish, as evidenced by the elevated plasma 3,3',5-triiodo-l-thyronine (p<0.05) and thyroid-stimulating hormone (p<0.01) levels as well as up-regulated hepatic and gonadal type I deiodinase (p<0.01), type II deiodinase (p<0.01) and thyroid receptor (p<0.05) mRNA levels. Thyroid disrupting potency decreased markedly as raw leachate progressed through the "membrane bioreactor + reverse osmosis" treatment but could still be detected in the treated leachate. As our results indicated, thyroid system in female goldfish was more sensitive to leachate exposure than that of the male fish.
[Mh] Termos MeSH primário: Disruptores Endócrinos/toxicidade
Expressão Gênica/efeitos dos fármacos
Carpa Dourada/sangue
Tireotropina/sangue
Tri-Iodotironina/sangue
Poluentes Químicos da Água/toxicidade
[Mh] Termos MeSH secundário: Animais
Reatores Biológicos
China
Feminino
Carpa Dourada/genética
Gônadas/efeitos dos fármacos
Gônadas/metabolismo
Iodeto Peroxidase/genética
Fígado/efeitos dos fármacos
Fígado/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Eliminação de Resíduos/métodos
Receptores alfa dos Hormônios Tireóideos/genética
Receptores beta dos Hormônios Tireóideos/genética
Tireotropina/genética
Tiroxina/sangue
Tiroxina/genética
Tri-Iodotironina/genética
Purificação da Água/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endocrine Disruptors); 0 (Thyroid Hormone Receptors alpha); 0 (Thyroid Hormone Receptors beta); 0 (Water Pollutants, Chemical); 06LU7C9H1V (Triiodothyronine); 9002-71-5 (Thyrotropin); EC 1.11.1.8 (Iodide Peroxidase); Q51BO43MG4 (Thyroxine)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170916
[Lr] Data última revisão:
170916
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161014
[St] Status:MEDLINE


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[PMID]:27732649
[Au] Autor:Cvoro A; Bajic A; Zhang A; Simon M; Golic I; Sieglaff DH; Maletic-Savatic M; Korac A; Webb P
[Ad] Endereço:Genomic Medicine, Houston Methodist Research Institute, Houston, TX, United States of America.
[Ti] Título:Ligand Independent and Subtype-Selective Actions of Thyroid Hormone Receptors in Human Adipose Derived Stem Cells.
[So] Source:PLoS One;11(10):e0164407, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thyroid hormone (TH) receptors (TRs α and ß) are homologous ligand-dependent transcription factors (TFs). While the TRs display distinct actions in development, metabolic regulation and other processes, comparisons of TRα and TRß dependent gene regulation mostly reveal similar mechanisms of action and few TR subtype specific genes. Here, we show that TRα predominates in multipotent human adipose derived stem cells (hADSC) whereas TRß is expressed at lower levels and is upregulated during hADSC differentiation. The TRs display several unusual properties in parental hADSC. First, TRs display predominantly cytoplasmic intracellular distribution and major TRα variants TRα1 and TRα2 colocalize with mitochondria. Second, knockdown experiments reveal that endogenous TRs influence hADSC cell morphology and expression of hundreds of genes in the absence of hormone, but do not respond to exogenous TH. Third, TRα and TRß affect hADSC in completely distinct ways; TRα regulates cell cycle associated processes while TRß may repress aspects of differentiation. TRα splice variant specific knockdown reveals that TRα1 and TRα2 both contribute to TRα-dependent gene expression in a gene specific manner. We propose that TRs work in a non-canonical and hormone independent manner in hADSC and that prominent subtype-specific activities emerge in the context of these unusual actions.
[Mh] Termos MeSH primário: Tecido Adiposo/citologia
Regulação da Expressão Gênica no Desenvolvimento
Células-Tronco/citologia
Receptores alfa dos Hormônios Tireóideos/metabolismo
Receptores beta dos Hormônios Tireóideos/metabolismo
[Mh] Termos MeSH secundário: Ciclo Celular
Diferenciação Celular
Linhagem Celular
Inativação Gênica
Seres Humanos
Células-Tronco/metabolismo
Receptores alfa dos Hormônios Tireóideos/análise
Receptores alfa dos Hormônios Tireóideos/genética
Receptores beta dos Hormônios Tireóideos/análise
Receptores beta dos Hormônios Tireóideos/genética
Tri-Iodotironina/análise
Tri-Iodotironina/genética
Tri-Iodotironina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Thyroid Hormone Receptors alpha); 0 (Thyroid Hormone Receptors beta); 06LU7C9H1V (Triiodothyronine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170529
[Lr] Data última revisão:
170529
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161013
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0164407


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[PMID]:27565560
[Au] Autor:Kot M; Daujat-Chavanieu M
[Ad] Endereço:Institute of Pharmacology, Polish Academy of Sciences, Smetna 12, 31-343 Kraków, Poland. Electronic address: kot@if-pan.krakow.pl.
[Ti] Título:The impact of serotonergic system dysfunction on the regulation of P4501A isoforms during liver insufficiency and consequences for thyroid hormone homeostasis.
[So] Source:Food Chem Toxicol;97:70-81, 2016 Nov.
[Is] ISSN:1873-6351
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:This study aimed to evaluate the impact of serotonergic system dysfunction on the regulation of cytochrome P4501A (CYP1A) during liver insufficiency. A rat model of liver insufficiency with a dysfunctional serotonergic system was developed. To induce liver insufficiency, animals were treated with nitrosodiethylamine (DEN) at 50 mg/kg of body weight twice a week for 7 weeks. To induce serotonergic system dysfunction, the animals were fed a tryptophan-free diet for 3 days. Serotonergic system dysfunction during liver insufficiency generated the aryl hydrocarbon receptor (AhR) activation and the "superinduction" of the AhR target genes: CYP1A1, CYP1B1 and UGT1A, with a concomitant increase in CYP1A1 protein and activity. CYP1A2 gene expression was simultaneously down-regulated, with a concomitant decrease in CYP1A2 protein and activity. A significant reduction in TRß receptor levels, together with a simultaneous increase of TRα receptor gene and protein level (mainly TRα2 isoform) after serotonergic system dysfunction, suggests that the serotoninergic system is involved in the regulation of CYP1A isoforms without influence from thyroid hormones during liver insufficiency. The interplay between the serotonergic system and the regulation of CYP1A isoforms, which are downstream targets of AhR activation, is dependent on hepatic function and can be observed without influence from thyroid hormones.
[Mh] Termos MeSH primário: Citocromo P-450 CYP1A1/genética
Citocromo P-450 CYP1A2/genética
Regulação Enzimológica da Expressão Gênica
Insuficiência Hepática/metabolismo
Hormônios Tireóideos/metabolismo
[Mh] Termos MeSH secundário: Alquilantes/toxicidade
Animais
Citocromo P-450 CYP1A1/metabolismo
Citocromo P-450 CYP1A2/metabolismo
Dietilnitrosamina/toxicidade
Glucuronosiltransferase/genética
Glucuronosiltransferase/metabolismo
Insuficiência Hepática/induzido quimicamente
Homeostase
Ratos
Receptores alfa dos Hormônios Tireóideos/genética
Receptores alfa dos Hormônios Tireóideos/metabolismo
Receptores beta dos Hormônios Tireóideos/genética
Receptores beta dos Hormônios Tireóideos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alkylating Agents); 0 (Thyroid Hormone Receptors alpha); 0 (Thyroid Hormone Receptors beta); 0 (Thyroid Hormones); 0 (Ugt1a1 protein, rat); 3IQ78TTX1A (Diethylnitrosamine); EC 1.14.14.1 (Cytochrome P-450 CYP1A1); EC 1.14.14.1 (Cytochrome P-450 CYP1A2); EC 2.4.1.17 (Glucuronosyltransferase)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170307
[Lr] Data última revisão:
170307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160828
[St] Status:MEDLINE



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