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[PMID]:29197138
[Au] Autor:Chen Y; Lu J; Xia L; Xue D; Yu X; Shen D; Xu L; Li G
[Ad] Endereço:Department of Urology and Chawnshang Chang Liver Cancer Center, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
[Ti] Título:Testicular orphan receptor 4 promotes tumor progression and implies poor survival through AKT3 regulation in seminoma.
[So] Source:Cancer Sci;109(2):384-394, 2018 Feb.
[Is] ISSN:1349-7006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Seminoma is the most common testicular germ cell tumor worldwide and mainly occurs in 15-35-year-old young men. Early studies have indicated that testicular nuclear receptor 4 (TR4) first cloned from testis is involved in the invasion and metastasis of several human tumors; however, little attention is paid to the function of TR4 in seminoma. Our immunohistochemical (IHC) staining results showed that patients with advanced stage tumors tended to have higher expression of TR4. Importantly, there was a significant association between elevated TR4 expression and reduced overall survival in seminoma patients. In vitro MTS, western blot and transwell assays, after manipulating TR4 expression in Tcam-2 cells, revealed that TR4 induced epithelial-to-mesenchymal transition (EMT) and promoted Tcam-2 cell proliferation and invasion. Mechanism dissection demonstrated that AKT3, a critical component in the signaling pathway, played a crucial role in mediating TR4-promoted Tcam-2 cell proliferation and invasion. We further revealed that TR4 modulated AKT3 at the transcriptional level via chromatin immunoprecipitation and luciferase assays. Meanwhile, addition of the AKT3 siRNA blocked the function of TR4. Overall, these findings first elucidate that TR4 is a novel prognostic marker and plays a critical role in the metastatic capacity of Tcam-2 cells by EMT regulation and, consequently, targeting TR4-AKT3 pathway may serve as a potential therapeutic approach for seminoma.
[Mh] Termos MeSH primário: Proteínas Proto-Oncogênicas c-akt/genética
Receptores de Esteroides/metabolismo
Receptores dos Hormônios Tireóideos/metabolismo
Seminoma/patologia
Neoplasias Testiculares/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Animais
Células COS
Linhagem Celular Tumoral
Proliferação Celular
Cercopithecus aethiops
Progressão da Doença
Transição Epitelial-Mesenquimal
Regulação Neoplásica da Expressão Gênica
Células HEK293
Seres Humanos
Masculino
Meia-Idade
Invasividade Neoplásica
Estadiamento de Neoplasias
Prognóstico
Proteínas Proto-Oncogênicas c-akt/metabolismo
Seminoma/genética
Seminoma/metabolismo
Transdução de Sinais
Neoplasias Testiculares/genética
Neoplasias Testiculares/metabolismo
Regulação para Cima
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NR2C2 protein, human); 0 (Receptors, Steroid); 0 (Receptors, Thyroid Hormone); EC 2.7.11.1 (AKT3 protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171203
[St] Status:MEDLINE
[do] DOI:10.1111/cas.13461


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[PMID]:28970022
[Au] Autor:Chang J; Hao W; Xu Y; Xu P; Li W; Li J; Wang H
[Ad] Endereço:Research Center for Eco-Environmental Science, Chinese Academy of Sciences, Shuangqing RD 18, Beijing 100085, China; University of Chinese Academy of Sciences, Yuquan RD 19 a, Beijing 100049, China.
[Ti] Título:Stereoselective degradation and thyroid endocrine disruption of lambda-cyhalothrin in lizards (Eremias argus) following oral exposure.
[So] Source:Environ Pollut;232:300-309, 2018 Jan.
[Is] ISSN:1873-6424
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The disturbance of the thyroid system and elimination of chiral pyrethroid pesticides with respect to enantioselectivity in reptiles have so far received limited attention by research. In this study, bioaccumulation, thyroid gland lesions, thyroid hormone levels, and hypothalamus-pituitary-thyroid axis-related gene expression in male Eremias argus were investigated after three weeks oral administration of lambda-cyhalothrin (LCT) enantiomers. In the lizard liver, the concentration of LCT was negatively correlated with the metabolite-3-phenoxybenzoic acid (PBA) level during 21 days of exposure. (+)-LCT exposure induced a higher thyroid follicular epithelium height than (-)-LCT exposure. The thyroxine levels were increased in both treated groups while only (+)-LCT exposure induced a significant change in the triiodothyronine (T3) level. In addition, the expressions of hypothalamus-pituitary-thyroid axis-related genes including thyroid hormone receptors (trs), deiodinases (dios), uridinediphosphate glucuronosyltransferase (udp), and sulfotransferase (sult) were up-regulated after exposure to the two enantiomers. (+)-LCT treatment resulted in higher expression of trs and (-)-LCT exposure led to greater stimulation of dios in the liver, which indicated PBA-induced antagonism on thyroid hormone receptors and LCT-induced disruption of thyroxine (T4) deiodination. The results suggest the (-)-LCT exposure causes higher residual level in lizard liver while induces less disruption on lizard thyroid activity than (+)-LCT.
[Mh] Termos MeSH primário: Lagartos/fisiologia
Nitrilos/toxicidade
Praguicidas/toxicidade
Piretrinas/toxicidade
Glândula Tireoide/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Benzoatos
Disruptores Endócrinos/metabolismo
Iodeto Peroxidase/metabolismo
Fígado/metabolismo
Lagartos/metabolismo
Masculino
Praguicidas/metabolismo
Receptores dos Hormônios Tireóideos/metabolismo
Estereoisomerismo
Glândula Tireoide/metabolismo
Hormônios Tireóideos/metabolismo
Tiroxina
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzoates); 0 (Endocrine Disruptors); 0 (Nitriles); 0 (Pesticides); 0 (Pyrethrins); 0 (Receptors, Thyroid Hormone); 0 (Thyroid Hormones); 69DC2655VH (3-phenoxybenzoic acid); EC 1.11.1.8 (Iodide Peroxidase); Q51BO43MG4 (Thyroxine); V0V73PEB8M (cyhalothrin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180122
[Lr] Data última revisão:
180122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE


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[PMID]:28743556
[Au] Autor:Martinez B; Scheibner M; Soñanez-Organis JG; Jaques JT; Crocker DE; Ortiz RM
[Ad] Endereço:Department of Molecular and Cellular Biology, University of California Merced, 5200 North Lake Road, Merced, CA 95343, USA. Electronic address: bmartinez26@ucmerced.edu.
[Ti] Título:Increased sensitivity of thyroid hormone-mediated signaling despite prolonged fasting.
[So] Source:Gen Comp Endocrinol;252:36-47, 2017 Oct 01.
[Is] ISSN:1095-6840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thyroid hormones (TH) can increase cellular metabolism. Food deprivation in mammals is typically associated with reduced thyroid gland responsiveness, in an effort to suppress cellular metabolism and abate starvation. However, in prolonged-fasted, elephant seal pups, cellular TH-mediated proteins are up-regulated and TH levels are maintained with fasting duration. The function and contribution of the thyroid gland to this apparent paradox is unknown and physiologically perplexing. Here we show that the thyroid gland remains responsive during prolonged food deprivation, and that its function and production of TH increase with fasting duration in elephant seals. We discovered that our modeled plasma TH data in response to exogenous thyroid stimulating hormone predicted cellular signaling, which was corroborated independently by the enzyme expression data. The data suggest that the regulation and function of the thyroid gland in the northern elephant seal is atypical for a fasted animal, and can be better described as, "adaptive fasting". Furthermore, the modeling data help substantiate the in vivo responses measured, providing unique insight on hormone clearance, production rates, and thyroid gland responsiveness. Because these unique endocrine responses occur simultaneously with a nearly strict reliance on the oxidation of lipid, these findings provide an intriguing model to better understand the TH-mediated reliance on lipid metabolism that is not otherwise present in morbidly obese humans. When coupled with cellular, tissue-specific responses, these data provide a more integrated assessment of thyroidal status that can be extrapolated for many fasting/food deprived mammals.
[Mh] Termos MeSH primário: Jejum/metabolismo
Focas Verdadeiras/metabolismo
Transdução de Sinais
Hormônios Tireóideos/metabolismo
[Mh] Termos MeSH secundário: Animais
Jejum/sangue
Iodeto Peroxidase/metabolismo
Modelos Biológicos
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptores dos Hormônios Tireóideos/metabolismo
Focas Verdadeiras/sangue
Hormônios Tireóideos/sangue
Hormônios Tireóideos/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (Receptors, Thyroid Hormone); 0 (Thyroid Hormones); EC 1.11.1.8 (Iodide Peroxidase)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171222
[Lr] Data última revisão:
171222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE


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[PMID]:28911178
[Au] Autor:Pinto VMS; Minakhina S; Qiu S; Sidhaye A; Brotherton MP; Suhotliv A; Wondisford FE
[Ad] Endereço:Division of Endocrinology, Department of Medicine, Escola Paulista de Medicina, Universidade Federal de São Paulo, 04021-001 São Paulo, Brazil.
[Ti] Título:Naturally Occurring Amino Acids in Helix 10 of the Thyroid Hormone Receptor Mediate Isoform-Specific TH Gene Regulation.
[So] Source:Endocrinology;158(9):3067-3078, 2017 Sep 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thyroid hormone (TH) action is mediated by the products of two genes, TH receptor (THR)α (THRA) and THRß (THRB) that encode several closely related receptor isoforms with differing tissue distributions. The vast majority of THR isoform-specific effects are thought to be due to tissue-specific differences in THR isoform expression levels. We investigated the alternative hypothesis that intrinsic functional differences among THR isoforms mediate these tissue-specific effects. To achieve the same level of expression of each isoform, we created tagged THR isoforms and tested their DNA and functional properties in vitro. We found significant homodimerization and functional differences among the THR isoforms. THRA1 was unable to form homodimers on direct repeat separated by 4 bp DNA elements and was also defective in TH-dependent repression of Tshb and Rxrg in a thyrotroph cell line, TαT1.1. In contrast, THRB2 was both homodimer sufficient and fully functional on these negatively regulated genes. Using domain exchanges and individual amino acid switches between THRA1 and THRB2, we identified three amino acids in helix 10 of the THRB2 ligand-binding domain that are required for negative regulation and are absent in THRA1.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica
Domínios e Motivos de Interação entre Proteínas/fisiologia
Receptores dos Hormônios Tireóideos/química
Receptores dos Hormônios Tireóideos/metabolismo
[Mh] Termos MeSH secundário: Aminoácidos/fisiologia
Animais
Células Cultivadas
Camundongos
Ligação Proteica
Domínios e Motivos de Interação entre Proteínas/genética
Isoformas de Proteínas
Multimerização Proteica
Estrutura Secundária de Proteína
Receptores dos Hormônios Tireóideos/genética
Hormônios Tireóideos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acids); 0 (Protein Isoforms); 0 (Receptors, Thyroid Hormone); 0 (Thyroid Hormones)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00314


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[PMID]:28893954
[Au] Autor:Nagaoka M; Yashiro T; Uchida Y; Ando T; Hara M; Arai H; Ogawa H; Okumura K; Kasakura K; Nishiyama C
[Ad] Endereço:Laboratory of Molecular Biology and Immunology, Department of Biological Science and Technology, Faculty of Industrial Science and Technology, Tokyo University of Science, Tokyo 125-8585, Japan; and.
[Ti] Título:The Orphan Nuclear Receptor NR4A3 Is Involved in the Function of Dendritic Cells.
[So] Source:J Immunol;199(8):2958-2967, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:NR4A3/NOR1 belongs to the NR4A subfamily of the nuclear hormone receptor superfamily, which is activated in a ligand-independent manner. To examine the role of NR4A3 in gene expression of dendritic cells (DCs), we introduced NR4A3 small interfering RNA (siRNA) into bone marrow-derived DCs and determined the expression levels of mRNA and proteins of cytokines, cell surface molecules, NF-κB signaling-related proteins, and transcription factors. The expression level of NR4A3 was markedly upregulated by TLR-mediated stimulation in DCs. NR4A3 knockdown significantly suppressed LPS, CpG, or poly(I:C)-mediated upregulation of CD80, CD86, IL-10, IL-6, and IL-12. Proliferation and IL-2 production levels of T cells cocultured with NR4A3 knocked-down DCs were significantly lower than that of T cells cocultured with control DCs. Furthermore, the expression of IKKß, IRF4, and IRF8 was significantly decreased in NR4A3 siRNA-introduced bone marrow-derived DCs. The knockdown experiments using siRNAs for IKKß, IRF4, and/or IRF8 indicated that LPS-induced upregulation of IL-10 and IL-6 was reduced in IKKß knocked-down cells, and that the upregulation of IL-12 was suppressed by the knockdown of IRF4 and IRF8. Taken together, these results indicate that NR4A3 is involved in TLR-mediated activation and gene expression of DCs.
[Mh] Termos MeSH primário: Diferenciação Celular
Proteínas de Ligação a DNA/metabolismo
Células Dendríticas/imunologia
Ativação Linfocitária
Proteínas do Tecido Nervoso/metabolismo
Receptores de Esteroides/metabolismo
Receptores dos Hormônios Tireóideos/metabolismo
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Apresentação do Antígeno
Proliferação Celular
Células Cultivadas
Técnicas de Cocultura
Proteínas de Ligação a DNA/genética
Lipopolissacarídeos/imunologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
NF-kappa B/metabolismo
Proteínas do Tecido Nervoso/genética
RNA Interferente Pequeno/genética
Receptores de Esteroides/genética
Receptores dos Hormônios Tireóideos/genética
Transdução de Sinais
Receptores Toll-Like/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (Lipopolysaccharides); 0 (NF-kappa B); 0 (Nerve Tissue Proteins); 0 (Nr4a3 protein, mouse); 0 (RNA, Small Interfering); 0 (Receptors, Steroid); 0 (Receptors, Thyroid Hormone); 0 (Toll-Like Receptors)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601911


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[PMID]:28781255
[Au] Autor:Shpakov AO
[Ad] Endereço:I.M. Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences.
[Ti] Título:[Pharmacological approaches for correction of thyroid dysfunctions in diabetes mellitus].
[Ti] Título:Farmakologicheskie podkhody dlia korrektsii disfunktsii shchitovidnoi zhelezy v usloviiakh sakharnogo diabeta..
[So] Source:Biomed Khim;63(3):219-231, 2017 May.
[Is] ISSN:2310-6972
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Thyroid diseases are closely associated with the development of types 1 and 2 diabetes mellitus (DM), and as a consequence, the development of effective approaches for their treatment is one of the urgent problems of endocrinology. Traditionally, thyroid hormones (TH) are used to correct functions of the thyroid system. However, they are characterized by many side effects, such as their negative effect on the cardiovascular system as well as the ability of TH to enhance insulin resistance and to disturb insulin-producing function of pancreas, exacerbating thereby diabetic pathology. Therefore, the analogues of TH, selective for certain types of TH receptors, that do not have these side effects, are being developed. The peptide and low-molecular weight regulators of thyroid-stimulating hormone receptor, which regulate the activity of the thyroid axis at the stage of TH synthesis and secretion in thyrocytes, are being created. Systemic and intranasal administration of insulin, metformin therapy and drugs with antioxidant activity are effective for the treatment of thyroid pathology in types 1 and 2 DM. In the review, the literature data and the results of own investigations on pharmacological approaches for the treatment and prevention of thyroid diseases in patients with types 1 and 2 DM are summarized and analyzed.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 1/tratamento farmacológico
Diabetes Mellitus Tipo 2/tratamento farmacológico
Hipotireoidismo/tratamento farmacológico
Insulina/uso terapêutico
Peptídeos/uso terapêutico
Hormônios Tireóideos/uso terapêutico
[Mh] Termos MeSH secundário: Antioxidantes/uso terapêutico
Diabetes Mellitus Tipo 1/complicações
Diabetes Mellitus Tipo 1/genética
Diabetes Mellitus Tipo 1/patologia
Diabetes Mellitus Tipo 2/complicações
Diabetes Mellitus Tipo 2/genética
Diabetes Mellitus Tipo 2/patologia
Expressão Gênica
Seres Humanos
Hipotireoidismo/complicações
Hipotireoidismo/genética
Hipotireoidismo/patologia
Resistência à Insulina
Metformina/uso terapêutico
Peptídeos/síntese química
Receptores dos Hormônios Tireóideos/agonistas
Receptores dos Hormônios Tireóideos/genética
Receptores dos Hormônios Tireóideos/metabolismo
Transdução de Sinais
Glândula Tireoide/efeitos dos fármacos
Glândula Tireoide/metabolismo
Glândula Tireoide/patologia
Hormônios Tireóideos/biossíntese
Hormônios Tireóideos/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antioxidants); 0 (Insulin); 0 (Peptides); 0 (Receptors, Thyroid Hormone); 0 (Thyroid Hormones); 9100L32L2N (Metformin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170808
[St] Status:MEDLINE
[do] DOI:10.18097/PBMC20176303219


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[PMID]:28658938
[Au] Autor:Tonyushkina KN; Krug S; Ortiz-Toro T; Mascari T; Karlstrom RO
[Ad] Endereço:Division of Pediatric Endocrinology, Baystate Children's Hospital, Baystate Health, Springfield, Massachusetts 01199.
[Ti] Título:Low Thyroid Hormone Levels Disrupt Thyrotrope Development.
[So] Source:Endocrinology;158(9):2774-2782, 2017 Sep 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Low thyroid hormone (TH) conditions caused by a variety of prenatal and perinatal problems have been shown to alter postnatal regulatory thyrotropin (TSH) responsiveness to TH in humans and rodents. The mechanisms underlying this pituitary TH resistance remain unknown. Here we use the evolutionarily conserved zebrafish model to examine the effects of low TH on thyrotrope development and function. Zebrafish were exposed to the goitrogen 6-propyl-2-thiouracil (PTU) to block TH synthesis, and this led to an approximately 50% increase in thyrotrope numbers and an 8- to 10-fold increase in tshb mRNA abundance in 2-week-old larvae and 1-month-old juveniles. Thyrotrope numbers returned to normal 3 weeks after cessation of PTU treatment, demonstrating that these effects were reversible and revealing substantial plasticity in pituitary-thyroid axis regulation. Using a T4 challenge assay, we found that development under low-TH conditions did not affect the ability of T4 to suppress tshb mRNA levels despite the thyrotrope hyperplasia that resulted from temporary low-TH conditions. Together, these studies show that low developmental TH levels can lead to changes in thyrotrope number and function, providing a possible cellular mechanism underlying elevated TSH levels seen in neonates with either permanent or transient congenital hypothyroidism.
[Mh] Termos MeSH primário: Hipófise/efeitos dos fármacos
Hipófise/embriologia
Hormônios Tireóideos/farmacologia
Tireotrofos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Contagem de Células
Diferenciação Celular/efeitos dos fármacos
Hipotireoidismo Congênito/complicações
Hipotireoidismo Congênito/embriologia
Hipotireoidismo Congênito/genética
Hipotireoidismo Congênito/patologia
Embrião não Mamífero
Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos
Organogênese/efeitos dos fármacos
Hipófise/citologia
Hipófise/patologia
Propiltiouracila/farmacologia
Receptores dos Hormônios Tireóideos/genética
Receptores dos Hormônios Tireóideos/metabolismo
Tireotrofos/citologia
Tireotrofos/fisiologia
Tireotropina Subunidade beta/genética
Peixe-Zebra/embriologia
Peixe-Zebra/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Thyroid Hormone); 0 (Thyroid Hormones); 0 (Thyrotropin, beta Subunit); 721M9407IY (Propylthiouracil)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170630
[St] Status:MEDLINE
[do] DOI:10.1210/en.2016-1935


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[PMID]:28638936
[Au] Autor:Gkikas D; Tsampoula M; Politis PK
[Ad] Endereço:Center for Basic Research, Biomedical Research Foundation of the Academy of Athens, 4 Soranou Efesiou Str, 115 27, Athens, Greece.
[Ti] Título:Nuclear receptors in neural stem/progenitor cell homeostasis.
[So] Source:Cell Mol Life Sci;74(22):4097-4120, 2017 Nov.
[Is] ISSN:1420-9071
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:In the central nervous system, embryonic and adult neural stem/progenitor cells (NSCs) generate the enormous variety and huge numbers of neuronal and glial cells that provide structural and functional support in the brain and spinal cord. Over the last decades, nuclear receptors and their natural ligands have emerged as critical regulators of NSC homeostasis during embryonic development and adult life. Furthermore, substantial progress has been achieved towards elucidating the molecular mechanisms of nuclear receptors action in proliferative and differentiation capacities of NSCs. Aberrant expression or function of nuclear receptors in NSCs also contributes to the pathogenesis of various nervous system diseases. Here, we review recent advances in our understanding of the regulatory roles of steroid, non-steroid, and orphan nuclear receptors in NSC fate decisions. These studies establish nuclear receptors as key therapeutic targets in brain diseases.
[Mh] Termos MeSH primário: Células-Tronco Neurais/metabolismo
Receptores Citoplasmáticos e Nucleares/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Seres Humanos
Doenças do Sistema Nervoso/metabolismo
Doenças do Sistema Nervoso/patologia
Células-Tronco Neurais/citologia
Neurogênese
Receptores de Calcitriol/metabolismo
Receptores Estrogênicos/metabolismo
Receptores de Glucocorticoides/metabolismo
Receptores de Mineralocorticoides/metabolismo
Receptores dos Hormônios Tireóideos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, Calcitriol); 0 (Receptors, Cytoplasmic and Nuclear); 0 (Receptors, Estrogen); 0 (Receptors, Glucocorticoid); 0 (Receptors, Mineralocorticoid); 0 (Receptors, Thyroid Hormone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1007/s00018-017-2571-4


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[PMID]:28617824
[Au] Autor:Sakane Y; Kanamoto N; Yamauchi I; Tagami T; Morita Y; Miura M; Sone M; Yasoda A; Kimura T; Nakao K; Inagaki N
[Ad] Endereço:Department of Diabetes, Endocrinology and Nutrition, Kyoto University Graduate School of Medicine, Kyoto, Japan.
[Ti] Título:Regulation of type 1 iodothyronine deiodinase by LXRα.
[So] Source:PLoS One;12(6):e0179213, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The iodothyronine deiodinases are selenoenzymes that regulate the activity of thyroid hormone via specific inner- or outer-ring deiodination. In humans, type 1 deiodinase (D1) is highly expressed in the liver, but the mechanism by which its gene expression is regulated remains to be elucidated. Liver X receptor α (LXRα), a transcription factor of the nuclear receptor superfamily, is highly expressed in the liver, where it functions as a sensor for excess intracellular oxysterols. LXRα interacts with other nuclear receptors on promoters of genes that contain a binding core sequence for nuclear receptors. In addition, it is reported that the promoter of the gene encoding human D1 (hDIO1) contains the core sequence for one of nuclear receptors, thyroid hormone receptor (TR). We investigated the involvement of LXRα in the regulation of hDIO1, in the liver. We performed hDIO1 promoter-reporter assays using a synthetic LXR agonist, T0901317, and compared promoter activity between a human liver carcinoma cell line, HepG2, and a clone of human embryonic kidney cells, TSA201. We defined the region between nucleotides -131 and -114, especially nucleotides -126 and -125, of the hDIO1 promoter as critical for basal and LXRα-mediated specific transcriptional activation in HepG2 cells. An increase in hDIO1 expression was observed in LXRα-stimulated cells, but absent in cycloheximide-treated cells, indicating that new protein synthesis is required for LXRα-mediated regulation of hDIO1. On the other hand, electrophoretic mobility shift assays revealed that LXRα and RXRα bound to the hDIO1 promoter. We also demonstrated that LXRα and TRß compete with each other on this specific region of the promoter. In conclusion, our results indicated that LXRα plays a specific and important role in activation of TH by regulating D1, and that LXRα binds to and regulates the hDIO1 promoter, competing with TRß on specific sequences within the promoter.
[Mh] Termos MeSH primário: Regulação Enzimológica da Expressão Gênica/fisiologia
Iodeto Peroxidase/biossíntese
Receptores X do Fígado/metabolismo
Fígado/metabolismo
Elementos de Resposta/fisiologia
Ativação Transcricional/fisiologia
[Mh] Termos MeSH secundário: Cicloeximida/farmacologia
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Células HEK293
Células Hep G2
Seres Humanos
Hidrocarbonetos Fluorados/farmacologia
Iodeto Peroxidase/genética
Receptores X do Fígado/genética
Receptores dos Hormônios Tireóideos/genética
Receptores dos Hormônios Tireóideos/metabolismo
Receptor X Retinoide alfa/genética
Receptor X Retinoide alfa/metabolismo
Sulfonamidas/farmacologia
Ativação Transcricional/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hydrocarbons, Fluorinated); 0 (Liver X Receptors); 0 (NR1H3 protein, human); 0 (Receptors, Thyroid Hormone); 0 (Retinoid X Receptor alpha); 0 (Sulfonamides); 0 (TO-901317); 98600C0908 (Cycloheximide); EC 1.11.1.- (iodothyronine deiodinase type I); EC 1.11.1.8 (Iodide Peroxidase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170913
[Lr] Data última revisão:
170913
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170616
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179213


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[PMID]:28576869
[Au] Autor:Groeneweg S; Peeters RP; Visser TJ; Visser WE
[Ad] Endereço:Department of Internal Medicine and Academic Center for Thyroid DiseasesErasmus University Medical Center, Rotterdam, The Netherlands.
[Ti] Título:Triiodothyroacetic acid in health and disease.
[So] Source:J Endocrinol;234(2):R99-R121, 2017 Aug.
[Is] ISSN:1479-6805
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Thyroid hormone (TH) is crucial for development and metabolism of many tissues. The physiological relevance and therapeutic potential of TH analogs have gained attention in the field for many years. In particular, the relevance and use of 3,3',5-triiodothyroacetic acid (Triac, TA ) has been explored over the last decades. Although TA closely resembles the bioactive hormone T , differences in transmembrane transport and receptor isoform-specific transcriptional activation potency exist. For these reasons, the application of TA as a treatment for resistance to TH (RTH) syndromes, especially MCT8 deficiency, is topic of ongoing research. This review is a summary of all currently available literature about the formation, metabolism, action and therapeutic applications of TA .
[Mh] Termos MeSH primário: Tri-Iodotironina/análogos & derivados
[Mh] Termos MeSH secundário: Animais
Metabolismo Basal/fisiologia
Transporte Biológico/fisiologia
Seres Humanos
Sistema Hipotálamo-Hipofisário/fisiologia
Receptores dos Hormônios Tireóideos/metabolismo
Glândula Tireoide/fisiologia
Tri-Iodotironina/metabolismo
Tri-Iodotironina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, Thyroid Hormone); 06LU7C9H1V (Triiodothyronine); 29OQ9EU4R1 (3,3',5-triiodothyroacetic acid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170604
[St] Status:MEDLINE
[do] DOI:10.1530/JOE-17-0113



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