Base de dados : MEDLINE
Pesquisa : A11.436.911 [Categoria DeCS]
Referências encontradas : 37 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 4 ir para página            

  1 / 37 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28743746
[Au] Autor:Citterio CE; Veluswamy B; Morgan SJ; Galton VA; Banga JP; Atkins S; Morishita Y; Neumann S; Latif R; Gershengorn MC; Smith TJ; Arvan P
[Ad] Endereço:From the Division of Metabolism, Endocrinology and Diabetes, University of Michigan Medical School, Ann Arbor, Michigan 48105.
[Ti] Título: triiodothyronine formation from thyrocytes activated by thyroid-stimulating hormone.
[So] Source:J Biol Chem;292(37):15434-15444, 2017 09 15.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The thyroid gland secretes primarily tetraiodothyronine (T ), and some triiodothyronine (T ). Under normal physiological circumstances, only one-fifth of circulating T is directly released by the thyroid, but in states of hyperactivation of thyroid-stimulating hormone receptors (TSHRs), patients develop a syndrome of relative T toxicosis. Thyroidal T production results from iodination of thyroglobulin (TG) at residues Tyr and Tyr , whereas thyroidal T production may originate in several different ways. In this study, the data demonstrate that within the carboxyl-terminal portion of mouse TG, T is formed independently of deiodination from T We found that upon iodination , T formation in TG was decreased in mice lacking TSHRs. Conversely, T that can be formed upon iodination of TG secreted from PCCL3 (rat thyrocyte) cells was augmented from cells previously exposed to increased TSH, a TSHR agonist, a cAMP analog, or a TSHR-stimulating antibody. We present data suggesting that TSH-stimulated TG phosphorylation contributes to enhanced T formation. These effects were reversed within a few days after removal of the hyperstimulating conditions. Indeed, direct exposure of PCCL3 cells to human serum from two patients with Graves' disease, but not control sera, led to secretion of TG with an increased intrinsic ability to form T upon iodination. Furthermore, TG secreted from human thyrocyte cultures hyperstimulated with TSH also showed an increased intrinsic ability to form T Our data support the hypothesis that TG processing in the secretory pathway of TSHR-hyperstimulated thyrocytes alters the structure of the iodination substrate in a way that enhances T formation, contributing to the relative T toxicosis of Graves' disease.
[Mh] Termos MeSH primário: Processamento de Proteína Pós-Traducional
Receptores da Tireotropina/agonistas
Transdução de Sinais
Tireoglobulina/metabolismo
Células Epiteliais da Tireóide/metabolismo
Tireotropina/metabolismo
Tri-Iodotironina/biossíntese
[Mh] Termos MeSH secundário: Animais
Proteínas de Ligação ao Cálcio/agonistas
Proteínas de Ligação ao Cálcio/genética
Proteínas de Ligação ao Cálcio/metabolismo
Caseína Quinase I/genética
Caseína Quinase I/metabolismo
Linhagem Celular
Células Cultivadas
Proteínas da Matriz Extracelular/agonistas
Proteínas da Matriz Extracelular/genética
Proteínas da Matriz Extracelular/metabolismo
Doença de Graves/sangue
Doença de Graves/metabolismo
Doença de Graves/patologia
Halogenação
Seres Humanos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fosforilação
Proteínas Serina-Treonina Quinases/química
Proteínas Serina-Treonina Quinases/genética
Proteínas Serina-Treonina Quinases/metabolismo
Ratos
Receptores da Tireotropina/genética
Receptores da Tireotropina/metabolismo
Tireoglobulina/secreção
Células Epiteliais da Tireóide/citologia
Células Epiteliais da Tireóide/patologia
Células Epiteliais da Tireóide/secreção
Tirosina/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Calcium-Binding Proteins); 0 (Extracellular Matrix Proteins); 0 (FAM20C protein, mouse); 0 (Receptors, Thyrotropin); 06LU7C9H1V (Triiodothyronine); 42HK56048U (Tyrosine); 9002-71-5 (Thyrotropin); 9010-34-8 (Thyroglobulin); EC 2.7.11.1 (Casein Kinase I); EC 2.7.11.1 (FAM20C protein, human); EC 2.7.11.1 (Fam20C protein, rat); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171230
[Lr] Data última revisão:
171230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.784447


  2 / 37 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28938449
[Au] Autor:Krieger CC; Perry JD; Morgan SJ; Kahaly GJ; Gershengorn MC
[Ad] Endereço:Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892.
[Ti] Título:TSH/IGF-1 Receptor Cross-Talk Rapidly Activates Extracellular Signal-Regulated Kinases in Multiple Cell Types.
[So] Source:Endocrinology;158(10):3676-3683, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We previously showed that thyrotropin (TSH)/insulinlike growth factor (IGF)-1 receptor cross-talk appears to be involved in Graves' orbitopathy (GO) pathogenesis and upregulation of thyroid-specific genes in human thyrocytes. In orbital fibroblasts from GO patients, coadministration of TSH and IGF-1 induces synergistic increases in hyaluronan secretion. In human thyrocytes, TSH plus IGF-1 synergistically increased expression of the sodium-iodide symporter that appeared to involve ERK1/2 activation. However, the details of ERK1/2 activation were not known, nor was whether ERK1/2 was involved in this synergism in other cell types. Using primary cultures of GO fibroblasts (GOFs) and human thyrocytes, as well as human embryonic kidney (HEK) 293 cells overexpressing TSH receptors (HEK-TSHRs), we show that simultaneous activation of TSHRs and IGF-1 receptors (IGF-1Rs) causes rapid, synergistic phosphorylation/activation of ERK1 and ERK2 in all three cell types. This effect is partially inhibited by pertussis toxin, an inhibitor of TSHR coupling to Gi/Go proteins. In support of a role for Gi/Go proteins in ERK1/2 phosphorylation, we found that knockdown of Gi(1-3) and Go in HEK-TSHRs inhibited ERK1/2 phosphorylation stimulated by TSH and TSH plus IGF-1. These data demonstrate that the synergistic effects of TSH plus IGF-1 occur early in the TSHR signaling cascade and further support the idea that TSHR/IGF-1R cross-talk is an important mechanism for regulation of human GOFs and thyrocytes.
[Mh] Termos MeSH primário: Fibroblastos/efeitos dos fármacos
Fator de Crescimento Insulin-Like I/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Receptor Cross-Talk
Receptor IGF Tipo 1/metabolismo
Receptores da Tireotropina/metabolismo
Tireotropina/farmacologia
[Mh] Termos MeSH secundário: Fibroblastos/metabolismo
Oftalmopatia de Graves
Células HEK293
Seres Humanos
Ácido Hialurônico/secreção
Proteína Quinase 1 Ativada por Mitógeno/efeitos dos fármacos
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/efeitos dos fármacos
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Fosforilação/efeitos dos fármacos
Simportadores/efeitos dos fármacos
Simportadores/metabolismo
Células Epiteliais da Tireóide/efeitos dos fármacos
Células Epiteliais da Tireóide/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Thyrotropin); 0 (Symporters); 0 (sodium-iodide symporter); 67763-96-6 (Insulin-Like Growth Factor I); 9002-71-5 (Thyrotropin); 9004-61-9 (Hyaluronic Acid); EC 2.7.10.1 (Receptor, IGF Type 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
[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:170923
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00528


  3 / 37 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28882636
[Au] Autor:Zhang Y; Wei F; Zhang J; Hao L; Jiang J; Dang L; Mei D; Fan S; Yu Y; Jiang L
[Ad] Endereço:Department of Endocrinology, Qilu Hospital, Shandong University, Jinan 250012, China; Department of Endocrinology, First Affiliated Hospital, Inner Mongolia University of Technology, Baotou 014010, China. Electronic address: zhangyonghonggogo@163.com.
[Ti] Título:Bisphenol A and estrogen induce proliferation of human thyroid tumor cells via an estrogen-receptor-dependent pathway.
[So] Source:Arch Biochem Biophys;633:29-39, 2017 Nov 01.
[Is] ISSN:1096-0384
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To determine the relationship between papillary thyroid carcinoma and environmental exposure to bisphenol A (BPA) or 17-ß estrogen (E ) by assessing the effects of these compounds on estrogen receptor expression and AKT/mTOR signaling. METHODS: The effects of low levels of BPA (1mM-10nM) and 17ß-estradiol (E2, 0.1mM-1nM) on ER expression and cellular proliferation were determined in human thyroid papillary cancer BHP10-3 cells. Protein and mRNA levels of estrogen nuclear receptors (ERα/ERß) and membrane receptors (GPR30) were determined by immunofluorescence assay, Western blotting, and RT-PCR, respectively, and proliferation was assessed by CCK-8 assay. RESULTS: The proliferative effects of BPA and E were both concentration- and time-dependent. Expression of ERα/ERß and GPR30 were enhanced by BPA and E BPA and E could quickly phosphorylate AKT/mTOR. Moreover, ICI suppressed ERα expression and activated GPR30 as did G-1. G-15 reversed the effects of E on GPR30 and AKT/mTOR, but did not alter the effect of BPA. CONCLUSIONS: BPA influences thyroid cancer proliferation by regulating expression of ERs and GPR30, a mechanism that differs from E . In addition, ICI and G-15 may have the potential to be used as anti-thyroid cancer agents.
[Mh] Termos MeSH primário: Poluentes Ocupacionais do Ar/farmacologia
Compostos Benzidrílicos/farmacologia
Estradiol/farmacologia
Receptor alfa de Estrogênio/genética
Receptor beta de Estrogênio/genética
Regulação Neoplásica da Expressão Gênica
Fenóis/farmacologia
Células Epiteliais da Tireóide/efeitos dos fármacos
[Mh] Termos MeSH secundário: Benzodioxóis/farmacologia
Ciclo Celular/efeitos dos fármacos
Ciclo Celular/genética
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Estradiol/análogos & derivados
Receptor alfa de Estrogênio/agonistas
Receptor alfa de Estrogênio/metabolismo
Receptor beta de Estrogênio/agonistas
Receptor beta de Estrogênio/metabolismo
Seres Humanos
Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-akt/genética
Proteínas Proto-Oncogênicas c-akt/metabolismo
Quinolinas/farmacologia
Receptores Estrogênicos/antagonistas & inibidores
Receptores Estrogênicos/genética
Receptores Estrogênicos/metabolismo
Receptores Acoplados a Proteínas-G/antagonistas & inibidores
Receptores Acoplados a Proteínas-G/genética
Receptores Acoplados a Proteínas-G/metabolismo
Transdução de Sinais
Serina-Treonina Quinases TOR/antagonistas & inibidores
Serina-Treonina Quinases TOR/genética
Serina-Treonina Quinases TOR/metabolismo
Células Epiteliais da Tireóide/metabolismo
Células Epiteliais da Tireóide/patologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-(6-bromo-1,3-benzodioxol-5-yl)-3a,4,5,9b-3H-cyclopenta(c)quinoline); 0 (Air Pollutants, Occupational); 0 (Benzhydryl Compounds); 0 (Benzodioxoles); 0 (Estrogen Receptor alpha); 0 (Estrogen Receptor beta); 0 (GPER protein, human); 0 (Phenols); 0 (Quinolines); 0 (Receptors, Estrogen); 0 (Receptors, G-Protein-Coupled); 0 (estrogen receptor alpha, human); 22X328QOC4 (fulvestrant); 4TI98Z838E (Estradiol); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); MLT3645I99 (bisphenol A)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE


  4 / 37 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28234980
[Au] Autor:Faria M; Matos P; Pereira T; Cabrera R; Cardoso BA; Bugalho MJ; Silva AL
[Ad] Endereço:Unidade de Investigação de Patobiologia Molecular, Instituto Português de Oncologia de Lisboa Francisco Gentil E.P.E., Lisboa, Portugal.
[Ti] Título:RAC1b overexpression stimulates proliferation and NF-kB-mediated anti-apoptotic signaling in thyroid cancer cells.
[So] Source:PLoS One;12(2):e0172689, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Overexpression of tumor-associated RAC1b has been recently highlighted as one of the most promising targets for therapeutic intervention in colon, breast, lung and pancreatic cancer. RAC1b is a hyperactive variant of the small GTPase RAC1 and has been recently shown to be overexpressed in a subset of papillary thyroid carcinomas associated with unfavorable outcome. Using the K1 PTC derived cell line as an in vitro model, we observed that both RAC1 and RAC1b were able to induce a significant increase on NF-kB and cyclin D1 reporter activity. A clear p65 nuclear localization was found in cells transfected with RAC1b-WT, confirming NF-kB canonical pathway activation. Consistently, we observed a RAC1b-mediated decrease in IκBα (NF-kB inhibitor) protein levels. Moreover, we show that RAC1b overexpression stimulates G1/S progression and protects thyroid cells against induced apoptosis, the latter through a process involving the NF-kB pathway. Present data support previous findings suggesting an important role for RAC1b in the development of follicular cell-derived thyroid malignancies and point out NF-kB activation as one of the molecular mechanisms associated with the pro-tumorigenic advantage of RAC1b overexpression in thyroid carcinomas.
[Mh] Termos MeSH primário: Regulação Neoplásica da Expressão Gênica
NF-kappa B/genética
Células Epiteliais da Tireóide/metabolismo
Proteínas rac1 de Ligação ao GTP/genética
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Apoptose/genética
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Ciclina D1/genética
Ciclina D1/metabolismo
Pontos de Checagem da Fase G1 do Ciclo Celular/efeitos dos fármacos
Seres Humanos
Inibidor de NF-kappaB alfa/genética
Inibidor de NF-kappaB alfa/metabolismo
NF-kappa B/metabolismo
Transdução de Sinais
Estaurosporina/farmacologia
Células Epiteliais da Tireóide/efeitos dos fármacos
Células Epiteliais da Tireóide/patologia
Transfecção
Proteínas rac1 de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCND1 protein, human); 0 (NF-kappa B); 0 (RAC1 protein, human); 136601-57-5 (Cyclin D1); 139874-52-5 (NF-KappaB Inhibitor alpha); EC 3.6.5.2 (rac1 GTP-Binding Protein); H88EPA0A3N (Staurosporine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170225
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0172689


  5 / 37 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28081700
[Au] Autor:Caselli E; D'Accolti M; Soffritti I; Zatelli MC; Rossi R; Degli Uberti E; Di Luca D
[Ad] Endereço:Department of Medical Sciences, Section of Microbiology and Medical Genetics, University of Ferrara, via L. Borsari 46, 44121, Ferrara, Italy. elisabetta.caselli@unife.it.
[Ti] Título:HHV-6A in vitro infection of thyrocytes and T cells alters the expression of miRNA associated to autoimmune thyroiditis.
[So] Source:Virol J;14(1):3, 2017 Jan 11.
[Is] ISSN:1743-422X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Human herpesviruses have been hypothesized as environmental triggers in the development of autoimmune thyroid diseases (AITD), and in particular active human herpesvirus 6A (HHV-6A) infection was detected in thyrocytes of Hashimoto's thyroiditis (HT) patients, who also show specific anti-viral immune responses. On the other hand, AITD patients display modulation of specific miRNAs in thyroid tissue and blood. We wanted to ascertain whether HHV-6A infection might be correlated to the miRNA dysregulation observed in AITD. METHODS: Human thyroid and T-cell lines were infected in vitro with HHV-6A,-6B or -7, and analysed for miRNAs expression, either by microarray or by specific RT-PCR assays detecting miRNAs associated with AITD in vivo. RESULTS: HHV-6A infection, but not -6B or -7 infections, induced a decrease in miR-155_2 expression and an increase in miR-1238 expression in thyrocytes, as well as an increase in the expression levels of several autoimmunity-associated miRNAs in T lymphocytes, including miR-16_1, miR34a, miR-130a, miR-143_1, miR-202, miR-301b, miR-302c, miR-449b, miR-451_1, and miR-1238_2. CONCLUSIONS: HHV-6A infection modulates miRNAs expression in the cell types involved in the development of AITD. Notably, our in vitro findings correlate with what observed in AITD patients, further supporting the association between HHV-6A infection and AITD development. Moreover, these effects are 6A-specific, emphasizing the differences between the two HHV-6 virus species, and suggesting diverse virus mechanisms of action and therapeutic approaches.
[Mh] Termos MeSH primário: Herpesvirus Humano 6/crescimento & desenvolvimento
MicroRNAs/análise
Linfócitos T/virologia
Células Epiteliais da Tireóide/virologia
Tireoidite Autoimune/patologia
[Mh] Termos MeSH secundário: Perfilação da Expressão Gênica
Herpesvirus Humano 7/crescimento & desenvolvimento
Seres Humanos
Análise em Microsséries
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MicroRNAs)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170823
[Lr] Data última revisão:
170823
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170114
[St] Status:MEDLINE
[do] DOI:10.1186/s12985-016-0672-6


  6 / 37 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28081504
[Au] Autor:Zhao C; Gao Y; Zhao L; Li Y; Zhang Y; Wang S; Zhang H; Lu G; Guo X
[Ad] Endereço:Department of Endocrinology, Peking University First Hospital, No. 8 Xi Shi Ku Street, Xi Cheng District, Beijing 100034, China.
[Ti] Título:The expression and function of the neonatal Fc receptor in thyrocytes of Hashimoto's thyroiditis.
[So] Source:Int Immunopharmacol;44:53-60, 2017 Mar.
[Is] ISSN:1878-1705
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Thyroglobulin (Tg) and thyroid peroxidase (TPO) antibodies (TgAb and TPOAb), which are primarily of the immunoglobulin G (IgG) class, can mediate antibody-dependent cell-mediated cytotoxicity in vitro. However, it is unclear whether any thyrocyte molecules can facilitate the transport and elimination of TgAb and TPOAb. The IgG transport receptor neonatal Fc receptor (FcRn) is a candidate mediator of these processes. In this study, we aimed to evaluate FcRn expression and function in normal and Hashimoto's thyroiditis (HT) thyrocytes. METHODS: FcRn expression in primary thyrocyte cultures (four normal and four HT groups) was examined by polymerase chain reaction (PCR) and Western blotting. Localization of FcRn was demonstrated by immunoelectron microscopy. A double immunofluorescence staining method was adopted to detect FcRn and internalized human TgAb IgG. Stimulation experiments were performed to assess the regulation of FcRn expression by T helper cell 1 (Th1) (IFN-γ and TNF-α) and Th2 cytokines (IL-10 and IL-4). RESULTS: FcRn expression was lower in HT thyrocytes than in normal thyrocytes. FcRn was located in the cytoplasm, membranes, mitochondria and transport vesicles of thyrocytes. Both human IgG and TgAb IgG were internalized by thyrocytes in a pH-dependent manner and co-localized with FcRn in thyrocytes. FcRn expression was downregulated by Th1 and Th2 cytokines in both normal and HT thyrocytes in a dose-dependent manner. CONCLUSIONS: Our results suggest that FcRn may be associated with the transport and metabolism of IgG in thyrocytes and that transport is independent of IgG type. FcRn may be involved in HT pathogenesis.
[Mh] Termos MeSH primário: Doença de Graves/metabolismo
Doença de Hashimoto/metabolismo
Antígenos de Histocompatibilidade Classe I/metabolismo
Receptores Fc/metabolismo
Células Epiteliais da Tireóide/metabolismo
[Mh] Termos MeSH secundário: Citotoxicidade Celular Dependente de Anticorpos
Células Cultivadas
Citocinas/metabolismo
Doença de Graves/imunologia
Doença de Hashimoto/imunologia
Células HeLa
Antígenos de Histocompatibilidade Classe I/genética
Seres Humanos
Imunoglobulina G/sangue
Iodeto Peroxidase/imunologia
Receptores Fc/genética
Tireoglobulina/imunologia
Células Epiteliais da Tireóide/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Fc receptor, neonatal); 0 (Histocompatibility Antigens Class I); 0 (Immunoglobulin G); 0 (Receptors, Fc); 9010-34-8 (Thyroglobulin); EC 1.11.1.8 (Iodide Peroxidase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170512
[Lr] Data última revisão:
170512
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170113
[St] Status:MEDLINE


  7 / 37 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27998776
[Au] Autor:Oda K; Luo Y; Yoshihara A; Ishido Y; Sekihata K; Usukura K; Sue M; Hiroi N; Hirose T; Suzuki K
[Ad] Endereço:Department of Clinical Laboratory Science, Faculty of Medical Technology, Teikyo University, 2-11-1 Kaga, Itabashi, Tokyo 173-8605, Japan; Laboratory of Molecular Diagnostics, Department of Mycobacteriology, Leprosy Research Center, National Institute of Infectious Diseases, 4-2-1 Aoba-cho, Higashim
[Ti] Título:Follicular thyroglobulin induces cathepsin H expression and activity in thyrocytes.
[So] Source:Biochem Biophys Res Commun;483(1):541-546, 2017 Jan 29.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thyroglobulin (Tg) stored in thyroid follicles exerts a potent negative-feedback effect on each step of pre-hormone biosynthesis, including Tg gene transcription and iodine uptake and organification, by suppressing the expression of specific transcription factors that regulate these steps. Pre-hormones are stored in the follicular colloid before being reabsorbed. Following lysosomal proteolysis of its precursor, thyroid hormone (TH) is released from thyroid follicles. Although the suppressive effects of follicular Tg on each step of pre-hormone biosynthesis have been extensively characterized, whether follicular Tg accumulation also affects hormone reabsorption, proteolysis, and secretion is unclear. In this study we explored whether follicular Tg can regulate the expression and function of the lysosomal endopeptidases cathepsins. We found that in the rat thyroid cell line FRTL-5 follicular Tg induced cathepsin H mRNA and protein expression, as well as cathepsin H enzyme activity. Double immunofluorescence staining showed that Tg endocytosis promoted cathepsin H translocalization into lysosomes where it co-localized with internalized Tg. These results suggest that cathepsin H is an active participant in lysosome-mediated pre-hormone degradation, and that follicular Tg stimulates mobilization of pre-hormones by activating cathepsin H-associated proteolysis pathways.
[Mh] Termos MeSH primário: Catepsina H/metabolismo
Tireoglobulina/metabolismo
Células Epiteliais da Tireóide/metabolismo
Glândula Tireoide/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Relação Dose-Resposta a Droga
Endocitose
Regulação da Expressão Gênica
Lisossomos/metabolismo
Microscopia de Fluorescência
RNA Mensageiro/metabolismo
Ratos
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 9010-34-8 (Thyroglobulin); EC 3.4.22.16 (Cathepsin H)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170606
[Lr] Data última revisão:
170606
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161222
[St] Status:MEDLINE


  8 / 37 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27941541
[Au] Autor:Rossi ED; Bizzarro T; Martini M; Larocca LM; Schmitt F; Vielh P
[Ad] Endereço:*Division of Anatomic Pathology and Histology, Catholic University of Sacred Heart, Rome, Italy †Instituto de Patologia e Imunologia Molecular da Universidade do Porto (IPATIMUP), Porto, Portugal ‡Department of Pathology, Laboratoire National de Santé, Dudelange, Luxembourg.
[Ti] Título:Cytopathology of Follicular Cell Nodules.
[So] Source:Adv Anat Pathol;24(1):45-55, 2017 Jan.
[Is] ISSN:1533-4031
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The detection of thyroid nodules, consisting of different diseases, represents a common finding in population. Their evaluation and diagnosis are mostly achieved with fine-needle aspiration cytology (FNAC). Even though the majority of thyroid nodules are correctly diagnosed, a total of 25% to 30% of them are classified "indeterminate" comprising lesions with varying risk of malignancy and different types of management. Although the number of thyroid FNACs, including small lesions, is increasing due to the reliance upon sonographic and cytologic interpretations, there are issues concerning cytomorphologic interpretation and interobserver reproducibility. Different classification systems have tried to better define the criteria for inclusion in specific categories and to therefore reduce the rate of indeterminate diagnoses such as atypia of undetermined significance, follicular neoplasms, and suspicious for malignancy. However, the support of ancillary techniques (eg, immunocytochemistry and molecular analysis) are reshaping morphologic diagnoses made on materials obtained from FNAC.
[Mh] Termos MeSH primário: Células Epiteliais da Tireóide/patologia
Nódulo da Glândula Tireoide/diagnóstico
Nódulo da Glândula Tireoide/patologia
[Mh] Termos MeSH secundário: Biópsia por Agulha Fina
Citodiagnóstico/métodos
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170119
[Lr] Data última revisão:
170119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161213
[St] Status:MEDLINE


  9 / 37 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27929668
[Au] Autor:Lee HJ; Lombardi A; Stefan M; Li CW; Inabnet WB; Owen RP; Concepcion E; Tomer Y
[Ad] Endereço:Division of Endocrinology, Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, New York.
[Ti] Título:CD40 Signaling in Graves Disease Is Mediated Through Canonical and Noncanonical Thyroidal Nuclear Factor κB Activation.
[So] Source:Endocrinology;158(2):410-418, 2017 02 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CD40, a tumor necrosis factor receptor, is a major immune-modulating susceptibility gene for Graves disease (GD) as well as for a variety of other autoimmune diseases. Its broad association with autoimmunity underscores its paramount role in the development of a normal adaptive immune response, primarily in coordinating effective antigen presentation. The molecular pathways by which CD40 activation in the thyroid induces GD are unknown. In this study, we investigated whether NF-κB, a ubiquitious family of transcription factors, mediates the downstream effects of thyroid-specific CD40 activation. Cultured primary human thyrocytes, from patients with and without GD, underwent CD40 stimulation. Once stimulated, cytokines and transcription factors specific for either the canonical nuclear factor κB (NF-κB)1 pathway [interleukin (IL)-6, IL-8, tumor necrosis factor (TNF)-α], which primarily recruits cells for innate immunity, or the noncanonical NF-κB2 pathway [B cell-activating factor of the TNF family, CC chemokine ligand (CCL)21], which directs B cell viability, were analyzed. Significant upregulation in the messenger RNA and protein levels of both canonical and noncanonical pathway cytokines was observed. Western blot analyses of the specific transcription factors for the NF-κB1 and NF-κB2 pathways (p65 and p100/p52, respectively) demonstrated that p65 is constitutively expressed. In contrast, CD40 stimulation robustly increased the expression of the NF-κB2 p52 transcription factor, and the upregulation was significantly more profound in the GD tissue than in the normal thyroid tissue. Our data show that CD40 activity in thyrocytes is prominently mediated via NF-κB and furthermore suggest that the NF-κB1 and NF-κB2 pathways both contribute to the triggering and the progression of GD.
[Mh] Termos MeSH primário: Antígenos CD40/metabolismo
Doença de Graves/etiologia
Subunidade p50 de NF-kappa B/metabolismo
Subunidade p52 de NF-kappa B/metabolismo
Células Epiteliais da Tireóide/metabolismo
[Mh] Termos MeSH secundário: Células Cultivadas
Doença de Graves/metabolismo
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD40 Antigens); 0 (NF-kappa B p50 Subunit); 0 (NF-kappa B p52 Subunit)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161209
[St] Status:MEDLINE
[do] DOI:10.1210/en.2016-1609


  10 / 37 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27876515
[Au] Autor:Hollenberg AN; Choi J; Serra M; Kotton DN
[Ad] Endereço:Division of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, United States. Electronic address: thollenb@bidmc.harvard.edu.
[Ti] Título:Regenerative therapy for hypothyroidism: Mechanisms and possibilities.
[So] Source:Mol Cell Endocrinol;445:35-41, 2017 Apr 15.
[Is] ISSN:1872-8057
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The ability to derive functional thyroid follicular cells from embryonic stem cells (ESCs) or induced pluripotent stem cells (iPSCs) would provide potential therapeutic benefit for patients with congenital or post-surgical hypothyroidism. Furthermore, understanding the process by which thyroid follicular cells develop will also provide great insight into the key steps that regulate the development of other tissues derived from endoderm. Here we review the advances in our understanding of the process of thyroid follicular cell development including the creation of two models that have allowed for the rescue of hypothyroid mouse recipients through the transplantation of thyroid follicular cells derived from mouse ESCs. Rapid progress in the field suggests that the same success should be achievable with human ESCs or iPSCs in the near future. Additionally, the availability of ESC or iPSC-derived thyroid follicular cell models will provide ideal systems to explore how genetic mutations, drugs or illness impact thyroid function in a cell-autonomous fashion.
[Mh] Termos MeSH primário: Células-Tronco Embrionárias/citologia
Hipotireoidismo/terapia
Células-Tronco Pluripotentes Induzidas/citologia
Células Epiteliais da Tireóide/transplante
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Transplante de Células
Seres Humanos
Camundongos
Medicina Regenerativa
Células Epiteliais da Tireóide/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161124
[St] Status:MEDLINE



página 1 de 4 ir para página            
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

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