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Pesquisa : D06.472.699.857 [Categoria DeCS]
Referências encontradas : 1029 [refinar]
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[PMID]:28929494
[Au] Autor:Pothoulakis C; Torre-Rojas M; Duran-Padilla MA; Gevorkian J; Zoras O; Chrysos E; Chalkiadakis G; Baritaki S
[Ad] Endereço:IBD Center, Division of Digestive Diseases, David Geffen School of Medicine at UCLA, Los Angeles, CA.
[Ti] Título:CRHR2/Ucn2 signaling is a novel regulator of miR-7/YY1/Fas circuitry contributing to reversal of colorectal cancer cell resistance to Fas-mediated apoptosis.
[So] Source:Int J Cancer;142(2):334-346, 2018 Jan 15.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Colorectal cancer (CRC) responds poorly to immuno-mediated cytotoxicity. Underexpression of corticotropin-releasing-hormone-receptor-2 (CRHR2) in CRC, promotes tumor survival, growth and Epithelial to Mesenchymal Transition (EMT), in vitro and in vivo. We explored the role of CRHR2 downregulation in CRC cell resistance to Fas/FasL-mediated apoptosis and the underlying molecular mechanism. CRC cell sensitivity to CH11-induced apoptosis was compared between Urocortin-2 (Ucn2)-stimulated parental and CRHR2-overexpressing CRC cell lines and targets of CRHR2/Ucn2 signaling were identified through in vitro and ex vivo analyses. Induced CRHR2/Ucn2 signaling in SW620 and DLD1 cells increased specifically their sensitivity to CH11-mediated apoptosis, via Fas mRNA and protein upregulation. CRC compared to control tissues had reduced Fas expression that was associated with lost CRHR2 mRNA, poor tumor differentiation and high risk for distant metastasis. YY1 silencing increased Fas promoter activity in SW620 and re-sensitized them to CH11-apoptosis, thus suggesting YY1 as a putative transcriptional repressor of Fas in CRC. An inverse correlation between Fas and YY1 expression was confirmed in CRC tissue arrays, while elevated YY1 mRNA was clinically relevant with advanced CRC grade and higher risk for distant metastasis. CRHR2/Ucn2 signaling downregulated specifically YY1 expression through miR-7 elevation, while miR-7 modulation in miR-7 SW620-CRHR2+ and miR-7 HCT116 cells, had opposite effects on YY1 and Fas expressions and cell sensitivity to CH11-killing. CRHR2/Ucn2 signaling is a negative regulator of CRC cell resistance to Fas/FasL-apoptosis via targeting the miR-7/YY1/Fas circuitry. CRHR2 restoration might prove effective in managing CRC response to immune-mediated apoptotic stimuli.
[Mh] Termos MeSH primário: Apoptose
Neoplasias Colorretais/patologia
Hormônio Liberador da Corticotropina/metabolismo
MicroRNAs/genética
Receptores de Hormônio Liberador da Corticotropina/metabolismo
Urocortinas/metabolismo
Fator de Transcrição YY1/metabolismo
Receptor fas/metabolismo
[Mh] Termos MeSH secundário: Proliferação Celular
Neoplasias Colorretais/genética
Neoplasias Colorretais/metabolismo
Hormônio Liberador da Corticotropina/genética
Transição Epitelial-Mesenquimal
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Receptores de Hormônio Liberador da Corticotropina/genética
Transdução de Sinais
Células Tumorais Cultivadas
Urocortinas/genética
Fator de Transcrição YY1/genética
Receptor fas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CRF receptor type 2); 0 (FAS protein, human); 0 (MIRN7 microRNA, human); 0 (MicroRNAs); 0 (Receptors, Corticotropin-Releasing Hormone); 0 (UCN2 protein, human); 0 (Urocortins); 0 (YY1 Transcription Factor); 0 (YY1 protein, human); 0 (fas Receptor); 9015-71-8 (Corticotropin-Releasing Hormone)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171214
[Lr] Data última revisão:
171214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.31064


  2 / 1029 MEDLINE  
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[PMID]:28550160
[Au] Autor:Tsuda T; Takefuji M; Wettschureck N; Kotani K; Morimoto R; Okumura T; Kaur H; Eguchi S; Sakaguchi T; Ishihama S; Kikuchi R; Unno K; Matsushita K; Ishikawa S; Offermanns S; Murohara T
[Ad] Endereço:Department of Cardiology, Nagoya University School of Medicine, Nagoya, Japan.
[Ti] Título:Corticotropin releasing hormone receptor 2 exacerbates chronic cardiac dysfunction.
[So] Source:J Exp Med;214(7):1877-1888, 2017 Jul 03.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Heart failure occurs when the heart is unable to effectively pump blood and maintain tissue perfusion. Despite numerous therapeutic advancements over previous decades, the prognosis of patients with chronic heart failure remains poor, emphasizing the need to identify additional pathophysiological factors. Here, we show that corticotropin releasing hormone receptor 2 (Crhr2) is a G protein-coupled receptor highly expressed in cardiomyocytes and continuous infusion of the Crhr2 agonist, urocortin 2 (Ucn2), reduced left ventricular ejection fraction in mice. Moreover, plasma Ucn2 levels were 7.5-fold higher in patients with heart failure compared to those in healthy controls. Additionally, cardiomyocyte-specific deletion of Crhr2 protected mice from pressure overload-induced cardiac dysfunction. Mice treated with a Crhr2 antagonist lost maladaptive 3'-5'-cyclic adenosine monophosphate (cAMP)-dependent signaling and did not develop heart failure in response to overload. Collectively, our results indicate that constitutive Crhr2 activation causes cardiac dysfunction and suggests that Crhr2 blockade is a promising therapeutic strategy for patients with chronic heart failure.
[Mh] Termos MeSH primário: Insuficiência Cardíaca/metabolismo
Miócitos Cardíacos/metabolismo
Receptores de Hormônio Liberador da Corticotropina/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Idoso
Animais
Western Blotting
Células Cultivadas
AMP Cíclico/metabolismo
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo
Feminino
Expressão Gênica
Insuficiência Cardíaca/sangue
Insuficiência Cardíaca/fisiopatologia
Seres Humanos
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Meia-Idade
Miócitos Cardíacos/efeitos dos fármacos
Receptores de Hormônio Liberador da Corticotropina/agonistas
Receptores de Hormônio Liberador da Corticotropina/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Urocortinas/sangue
Urocortinas/farmacologia
Função Ventricular Esquerda/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CRF receptor type 2); 0 (Cyclic AMP Response Element-Binding Protein); 0 (Receptors, Corticotropin-Releasing Hormone); 0 (Urocortins); E0399OZS9N (Cyclic AMP)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170528
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20161924


  3 / 1029 MEDLINE  
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[PMID]:28539353
[Au] Autor:Williams TA; Bergstrome JC; Scott J; Bernier NJ
[Ad] Endereço:Department of Integrative Biology, University of Guelph, Guelph, Ontario, Canada.
[Ti] Título:CRF and urocortin 3 protect the heart from hypoxia/reoxygenation-induced apoptosis in zebrafish.
[So] Source:Am J Physiol Regul Integr Comp Physiol;313(2):R91-R100, 2017 Aug 01.
[Is] ISSN:1522-1490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Fish routinely experience environmental hypoxia and have evolved various strategies to tolerate this challenge. Given the key role of the CRF system in coordinating the response to stressors and its cardioprotective actions against ischemia in mammals, we sought to characterize the cardiac CRF system in zebrafish and its role in hypoxia tolerance. We established that all genes of the CRF system, the ligands CRFa, CRFb, urotensin 1 (UTS1), and urocortin 3 (UCN3); the two receptor subtypes (CRFR1 and CRFR2); and the binding protein (CRFBP) are expressed in the heart of zebrafish: > > > > > In vivo, exposure to 5% O saturation for 15 min and 90 min of recovery resulted in four- to five-fold increases in whole heart and mRNA levels but did not affect the gene expression of other CRF system components. In vitro, as assessed by monitoring caspase 3 activity and the number of terminal deoxynucleotidyl transferase dUTP nick-end labeling-positive cells, pretreatment of excised whole hearts with CRF or UCN3 for 30 min prevented the increase in apoptosis associated with exposure to 1% O saturation for 30 min with a 24-h recovery. Lastly, the addition of the nonselective CRF receptor antagonist αh-CRF prevented the cytoprotective effects of CRF. We show that the CRF system is expressed in fish heart, is upregulated by hypoxia, and is cytoprotective. These findings identify a novel role for the CRF system in fish and a new strategy to tolerate hypoxia.
[Mh] Termos MeSH primário: Apoptose
Hormônio Liberador da Corticotropina/metabolismo
Coração/fisiopatologia
Traumatismo por Reperfusão Miocárdica/fisiopatologia
Urocortinas/metabolismo
Peixe-Zebra/fisiologia
[Mh] Termos MeSH secundário: Animais
Masculino
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Urocortins); 9015-71-8 (Corticotropin-Releasing Hormone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1152/ajpregu.00045.2017


  4 / 1029 MEDLINE  
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[PMID]:28380380
[Au] Autor:van der Meulen T; Mawla AM; DiGruccio MR; Adams MW; Nies V; Dólleman S; Liu S; Ackermann AM; Cáceres E; Hunter AE; Kaestner KH; Donaldson CJ; Huising MO
[Ad] Endereço:Department of Neurobiology, Physiology, and Behavior, College of Biological Sciences, University of California, Davis, Davis, CA 95616, USA.
[Ti] Título:Virgin Beta Cells Persist throughout Life at a Neogenic Niche within Pancreatic Islets.
[So] Source:Cell Metab;25(4):911-926.e6, 2017 Apr 04.
[Is] ISSN:1932-7420
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Postnatal maintenance or regeneration of pancreatic beta cells is considered to occur exclusively via the replication of existing beta cells, but clinically meaningful restoration of human beta cell mass by proliferation has never been achieved. We discovered a population of immature beta cells that is present throughout life and forms from non-beta precursors at a specialized micro-environment or "neogenic niche" at the islet periphery. These cells express insulin, but lack other key beta cell markers, and are transcriptionally immature, incapable of sensing glucose, and unable to support calcium influx. They constitute an intermediate stage in the transdifferentiation of alpha cells to cells that are functionally indistinguishable from conventional beta cells. We thus identified a lifelong source of new beta cells at a specialized site within healthy islets. By comparing co-existing immature and mature beta cells within healthy islets, we stand to learn how to mature insulin-expressing cells into functional beta cells.
[Mh] Termos MeSH primário: Envelhecimento/fisiologia
Microambiente Celular
Células Secretoras de Insulina/citologia
[Mh] Termos MeSH secundário: Adulto
Diferenciação Celular/genética
Transdiferenciação Celular
Diabetes Mellitus Tipo 1/metabolismo
Diabetes Mellitus Tipo 1/patologia
Perfilação da Expressão Gênica
Glucagon/metabolismo
Células Secretoras de Glucagon/metabolismo
Células Secretoras de Glucagon/patologia
Seres Humanos
Insulina/metabolismo
Células Secretoras de Insulina/metabolismo
Doadores de Tecidos
Transcrição Genética
Urocortinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insulin); 0 (Ucn3 protein, mouse); 0 (Urocortins); 9007-92-5 (Glucagon)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170406
[St] Status:MEDLINE


  5 / 1029 MEDLINE  
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[PMID]:28315311
[Au] Autor:Bagosi Z; Karasz G; Czébely-Lénárt A; Csabafi K; Jászberényi M; Telegdy G
[Ad] Endereço:Department of Pathophysiology, Faculty of Medicine, University of Szeged, Hungary. Electronic address: bagosi.zsolt@med.u-szeged.hu.
[Ti] Título:The effects of CRF and urocortins on the sociability of mice.
[So] Source:Brain Res;1663:114-122, 2017 May 15.
[Is] ISSN:1872-6240
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The aim of our study was to determine the role of corticotropin-releasing factor (CRF), the urocortins (Ucn1, Ucn2 and Ucn3) and their receptors (CRF and CRF ) in the sociability of mice. Male CFLP mice were administered intracerebroventricularly (icv) with CRF and urocortins alone or in combination with antalarmin (specific CRF antagonist) and astressin (specific CRF antagonist) and then investigated in a Crawley social interaction test arena, that consists of three chambers. An unknown male in a cage was put in the first chamber and an empty cage was put in the opposite chamber. The tested male was habituated with the middle chamber for 5min and then allowed to explore the remaining chambers for 5min, during which the number of entries and the time of interaction were measured. Intracerebroventricular administration of CRF decreased significantly the number of entries and the time of interaction with the unknown male and these effects were blocked by antalarmin, but not astressin . In contrast, central administration of Ucn1 increased significantly the number of entries into the chamber of the unknown male, without changing the time of interaction and this effect was blocked by astressin , but not antalarmin. Central administration of Ucn2 and Ucn3 didn't influence remarkably the number of entries, but it reduced the time of interaction between the male mice. Our study suggests that CRF and Ucn1 may play important, but different roles in sociability, and that Ucn2 and Ucn3, playing similar roles, must be also involved in social interactions.
[Mh] Termos MeSH primário: Hormônio Liberador da Corticotropina/metabolismo
Hormônio Liberador da Corticotropina/farmacologia
Urocortinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Comportamento Animal/efeitos dos fármacos
Hormônio Liberador da Corticotropina/efeitos dos fármacos
Masculino
Camundongos
Fragmentos de Peptídeos
Peptídeos Cíclicos
Pirimidinas
Pirróis
Receptores de Hormônio Liberador da Corticotropina/metabolismo
Comportamento Social
Urocortinas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CRF receptor type 1); 0 (CRF receptor type 2); 0 (Peptide Fragments); 0 (Peptides, Cyclic); 0 (Pyrimidines); 0 (Pyrroles); 0 (Receptors, Corticotropin-Releasing Hormone); 0 (Urocortins); 0 (antalarmin); 0 (astressin-2B); 9015-71-8 (Corticotropin-Releasing Hormone)
[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:170319
[St] Status:MEDLINE


  6 / 1029 MEDLINE  
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[PMID]:28302012
[Au] Autor:Rodriguez FD; Coveñas R
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Group GIR-BMD, Faculty of Chemistry, University of Salamanca, 37001 Salamanca. Spain.
[Ti] Título:Targeting NPY, CRF/UCNs and NPS Neuropeptide Systems to Treat Alcohol Use Disorder (AUD).
[So] Source:Curr Med Chem;24(23):2528-2558, 2017.
[Is] ISSN:1875-533X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The term Alcohol Use Disorder (AUD) incorporates different states of disease related to the recurrent use of alcohol and linked to the relevant impairment, disability and failure to perform major responsibilities in different realms. Many neurotransmitter systems are involved in the phases or states of alcoholism from reward mechanisms, associated to binge intoxication, to stress and anxiety linked to relapse and withdrawal. Some neuropeptides play a key function in the control of anxiety and stress, and establish a close relationship with the pathological mechanisms underlying alcohol addiction. Among them, Neuropeptide Y (NPY), Corticotropin-releasing factor (CRF)/Urocortins and Neuropeptide S (NPS) cross-talk, and are responsible for some of the maladaptation processes that the brain exhibits during the progression of the disease. METHOD: In this study, we review the literature mainly focused on the participation of these neuropeptides in the pathophysiology of AUD, as well as on the use of antagonists designed to investigate signaling mechanisms initiated after ligand binding and their connection to biochemical adaptation events coupled to alcohol addiction. The possibility that these systems may serve as therapeutic objectives to mitigate or eliminate the harm that drinking ethanol generates, is also discussed. CONCLUSION: The peptide systems reviewed here, together with other neurotransmitter systems and their mutual relationships, are firm candidates to be targeted to treat AUD.
[Mh] Termos MeSH primário: Consumo de Bebidas Alcoólicas/tratamento farmacológico
Transtornos Relacionados ao Uso de Álcool/tratamento farmacológico
Hormônio Liberador da Corticotropina/antagonistas & inibidores
Neuropeptídeo Y/antagonistas & inibidores
Neuropeptídeos/antagonistas & inibidores
Urocortinas/antagonistas & inibidores
[Mh] Termos MeSH secundário: Consumo de Bebidas Alcoólicas/metabolismo
Transtornos Relacionados ao Uso de Álcool/metabolismo
Animais
Hormônio Liberador da Corticotropina/metabolismo
Seres Humanos
Neuropeptídeo Y/metabolismo
Neuropeptídeos/metabolismo
Urocortinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Neuropeptide Y); 0 (Neuropeptides); 0 (Urocortins); 0 (neuropeptide S, human); 9015-71-8 (Corticotropin-Releasing Hormone)
[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:170318
[St] Status:MEDLINE
[do] DOI:10.2174/0929867324666170316120836


  7 / 1029 MEDLINE  
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[PMID]:28267582
[Au] Autor:Füredi N; Nagy Á; Mikó A; Berta G; Kozicz T; Pétervári E; Balaskó M; Gaszner B
[Ad] Endereço:Department of Anatomy, Medical School, University of Pécs, Hungary.
[Ti] Título:Melanocortin 4 receptor ligands modulate energy homeostasis through urocortin 1 neurons of the centrally projecting Edinger-Westphal nucleus.
[So] Source:Neuropharmacology;118:26-37, 2017 May 15.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The role of the urocortin 1 (Ucn1) expressing centrally projecting Edinger-Westphal (EWcp) nucleus in energy homeostasis and stress adaptation response has previously been investigated. Morphological and functional studies have proven that orexigenic and anorexigenic peptidergic afferents and receptors for endocrine messengers involved in the energy homeostasis are found in the EWcp. The central role of the hypothalamic melanocortin system in energy homeostasis is well known, however, no data have been published so far on possible crosstalk between melanocortins and EWcp-Ucn1. First, we hypothesized that members of the melanocortin system [i.e. alpha-melanocyte stimulating hormone (alpha-MSH), agouti-related peptide (AgRP), melanocortin 4 receptor (MC4R)] would be expressed in the EWcp. Second, we put forward, that alpha-MSH and AgRP contents as well as neuronal activity and Ucn1 peptide content of the EWcp would be affected by fasting. Third, we assumed that the intra-EWcp injections of exogenous MC4R agonists and antagonist would cause food intake-related and metabolic changes. Ucn1 neurons were found to carry MC4Rs, and they were contacted both by alpha-MSH and AgRP immunoreactive nerve fibers in the rat. The alpha-MSH immunosignal was reduced, while that of AgRP was increased upon starvation. These were associated with the elevation of FosB and Ucn1 expression. The intra-EWcp administration of MC4R blocker (i.e. HS024) had a similar, but enhanced effect on FosB and Ucn1. Furthermore, alpha-MSH injected into the EWcp had anorexigenic effect, increased oxygen consumption and caused peripheral vasodilation. We conclude that the melanocortin system influences the EWcp that contributes to energy-homeostasis.
[Mh] Termos MeSH primário: Núcleo de Edinger-Westphal/citologia
Homeostase/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Consumo de Oxigênio/efeitos dos fármacos
Receptor Tipo 4 de Melanocortina
Urocortinas/metabolismo
[Mh] Termos MeSH secundário: Proteína Relacionada com Agouti/metabolismo
Animais
Temperatura Corporal/efeitos dos fármacos
Vias de Administração de Medicamentos
Ingestão de Alimentos/efeitos dos fármacos
Jejum
Ligantes
Masculino
Fibras Nervosas/efeitos dos fármacos
Fibras Nervosas/fisiologia
Proteínas Oncogênicas v-fos/metabolismo
Peptídeos Cíclicos/farmacologia
Ratos
Ratos Wistar
Receptor Tipo 4 de Melanocortina/agonistas
Receptor Tipo 4 de Melanocortina/antagonistas & inibidores
Receptor Tipo 4 de Melanocortina/metabolismo
alfa-MSH/metabolismo
alfa-MSH/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AGRP protein, rat); 0 (Agouti-Related Protein); 0 (HS 024); 0 (Ligands); 0 (Oncogene Proteins v-fos); 0 (Peptides, Cyclic); 0 (Receptor, Melanocortin, Type 4); 0 (Urocortins); 581-05-5 (alpha-MSH)
[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:170308
[St] Status:MEDLINE


  8 / 1029 MEDLINE  
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[PMID]:28100871
[Au] Autor:Yang XF; Ren LW; Yang L; Deng CY; Li FR
[Ad] Endereço:The Key Laboratory of Stem Cell and Cellular Therapy, The Second Clinical Medical College (Shenzhen People's Hospital), Ji'nan University, Shenzhen, China.
[Ti] Título:In vivo direct reprogramming of liver cells to insulin producing cells by virus-free overexpression of defined factors.
[So] Source:Endocr J;64(3):291-302, 2017 Mar 31.
[Is] ISSN:1348-4540
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Direct reprogramming of autologous cells from diabetes patients to insulin producing cells is a new method for pancreatic cell replacement therapy. At present, transdifferentiation among mature cells is achieved mainly by introducing foreign genes into the starting tissue with viral vector, but there are potentical safety problems. In the present study, we delivered plasmids carrying Pdx1, Neurog3 and MafA genes (PNM) into mouse hepatocytes by hydrodynamics tail vein injection, investigated islet ß cells markers in transfected cells from protein and mRNA level, and then observed the long-term control of blood glucose in diabetic mice. We found that hepatocytes could be directly reprogrammed into insulin-producing cells after PNM gene transfection by non-viral hydrodynamics injection, and fasting blood glucose was reduced to normal, and lasted until 100 days after transfection. Intraperitoneal glucose tolerance test (IPGTT) showed that glucose regulation ability was improved gradually and the serum insulin level approached to the level of normal mice with time. Insulin-positive cells were found in the liver tissue, and the expression of various islet ß-cell-specific genes were detected at the mRNA level, including islet mature marker gene Ucn3. In conclusion, we provide a new approach for the treatment of diabetes by in vivo direct reprogramming of liver cells to insulin producing cells through non-viral methods.
[Mh] Termos MeSH primário: Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo
Transdiferenciação Celular
Hepatócitos/patologia
Proteínas de Homeodomínio/metabolismo
Células Secretoras de Insulina/patologia
Fatores de Transcrição Maf Maior/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Transativadores/metabolismo
Regulação para Cima
[Mh] Termos MeSH secundário: Animais
Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Biomarcadores/sangue
Biomarcadores/metabolismo
Glicemia/análise
Diabetes Mellitus Experimental/sangue
Diabetes Mellitus Experimental/metabolismo
Diabetes Mellitus Experimental/patologia
Diabetes Mellitus Experimental/terapia
Técnicas de Transferência de Genes/efeitos adversos
Hepatócitos/metabolismo
Hepatócitos/secreção
Proteínas de Homeodomínio/genética
Hidrodinâmica
Injeções Intravenosas
Insulina/sangue
Insulina/metabolismo
Insulina/secreção
Células Secretoras de Insulina/metabolismo
Células Secretoras de Insulina/secreção
Fatores de Transcrição Maf Maior/genética
Masculino
Camundongos Endogâmicos C57BL
Proteínas do Tecido Nervoso/genética
Plasmídeos/administração & dosagem
RNA Mensageiro/metabolismo
Organismos Livres de Patógenos Específicos
Cauda
Transativadores/genética
Urocortinas/genética
Urocortinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Biomarkers); 0 (Blood Glucose); 0 (Homeodomain Proteins); 0 (Insulin); 0 (Maf Transcription Factors, Large); 0 (Mafa protein, mouse); 0 (Nerve Tissue Proteins); 0 (Neurog3 protein, mouse); 0 (RNA, Messenger); 0 (Trans-Activators); 0 (Ucn3 protein, mouse); 0 (Urocortins); 0 (pancreatic and duodenal homeobox 1 protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170120
[St] Status:MEDLINE
[do] DOI:10.1507/endocrj.EJ16-0463


  9 / 1029 MEDLINE  
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[PMID]:27884738
[Au] Autor:Yamaguchi K
[Ad] Endereço:Department of Pathology, Dokkyo University School of Medicine, 880 Kitakobayashi, Mibu, Tochigi 321-0293, Japan. Electronic address: katsuyukiy@cc9.ne.jp.
[Ti] Título:Development of the human oculomotor nuclear complex: Centrally-projecting Edinger-Westphal nucleus.
[So] Source:Neurosci Lett;646:8-14, 2017 Apr 12.
[Is] ISSN:1872-7972
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The cytoarchitecturally defined Edinger-Westphal nucleus (EW) is now referred to by many investigators as the centrally-projecting EW (EWcp) in humans. Although the mature structure is well-characterized, there have been few reports describing the precise morphology of this nucleus during the second half of gestation. SUBJECTS/DESIGN: Eleven brains were examined from preterm infants, aged 20-39 postmenstrual weeks, who died of various causes. After fixation, the brains were embedded in celloidin and serial sections of 30-µm thickness were cut in the horizontal plane. Sections were stained using the Klüver-Barrera method. In addition to microscopic observations, computerized 3D reconstruction and morphometry were performed. RESULTS: From 21 weeks, the EWcp had a distinctive, complex 3D structure comprising two or three parts. The dorsal part was arcuate, half encircling the oculomotor somatic nuclei (OSN). The rostral part was the most voluminous, ventral to the rostral OSN, extending anteriorly. The caudal part was the smallest, and was composed of several neuronal groups near the ventral tip of the OSN. In three cases, the caudal part was absent. It could also be joined to the rostral part, forming a ventral part. The total volume of the EWcp increased exponentially with age, and the ventral part grew more rapidly than the dorsal part. The mean neuronal profile area increased linearly with age, and the rate of increase was almost equal between the dorsal and ventral parts. CONCLUSIONS: This study suggests that a distinctive, complex, two- or three-part 3D structure of the EWcp is preserved after mid-gestation, and that the ventral part of the EWcp may expand in volume more rapidly than the dorsal part.
[Mh] Termos MeSH primário: Núcleo de Edinger-Westphal/patologia
Neurônios/metabolismo
Nervo Oculomotor/patologia
Complexo Nuclear Oculomotor/patologia
[Mh] Termos MeSH secundário: Núcleo de Edinger-Westphal/crescimento & desenvolvimento
Seres Humanos
Nervo Oculomotor/metabolismo
Complexo Nuclear Oculomotor/crescimento & desenvolvimento
Urocortinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (UCN1 protein, human); 0 (Urocortins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161126
[St] Status:MEDLINE


  10 / 1029 MEDLINE  
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[PMID]:27841039
[Au] Autor:Temur M; Yilmaz Ö; Aksun S; Calan M; Özün Özbay P; Kumbasar S; Sever E
[Ad] Endereço:a Department of Obstetrics and Gynecology , Manisa Merkezefendi Hospital , Manisa , Turkey.
[Ti] Título:The relationship of urocortin-2 with insulin resistance patients having PCOS.
[So] Source:Gynecol Endocrinol;33(2):124-127, 2017 Feb.
[Is] ISSN:1473-0766
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In this study, we aimed to compare the serum urocortin-2 (UCN2) levels in women with polycystic ovary syndrome (PCOS) and healthy women. Thirty-eight patients with PCOS and 41 healthy women were included in the study whose age and BMI matched. The fasting serum glucose, insulin, free testosterone, hs-CRP and UCN2 levels of the all participants were examined. HOMA-IR formula was used in order to calculate the insulin resistance. Circulating UCN2 levels were significantly elevated in women with PCOS compared with controls (142.93 ± 59.48 versus 98.56 ± 65.01 pg/ml, p = 0.002). FBG, serum insulin, hs-CRP and HOMA-IR levels were found to be increased in women with PCOS. There was a positive correlation between UCN2 and free-testosterone in only PCOS group (r = 0.235, p = 0.027). Multivariate logistic regression analyses revealed that the odds ratio for PCOS was 2.31 for patients in the highest quartile of UCN2 compared with those in the lowest quartile (OR = 2.31, 95% CI = 1.88-2.83, p=0.021). Multiple linear regression analysis revealed that HOMA-IR, hs-CRP and free-testosterone independently predicted UCN2 levels (p < 0.05). UCN2 levels were significantly higher in PCOS cases when compared to control group. UCN2 is thought to be effective on pathophysiology of PCOS by paracrine and autocrine pathways.
[Mh] Termos MeSH primário: Proteína C-Reativa/metabolismo
Hormônio Liberador da Corticotropina/sangue
Resistência à Insulina
Síndrome do Ovário Policístico/sangue
Testosterona/sangue
Urocortinas/sangue
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (UCN2 protein, human); 0 (Urocortins); 3XMK78S47O (Testosterone); 9007-41-4 (C-Reactive Protein); 9015-71-8 (Corticotropin-Releasing Hormone)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170605
[Lr] Data última revisão:
170605
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161115
[St] Status:MEDLINE
[do] DOI:10.1080/09513590.2016.1240772



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