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Pesquisa : D12.776.631.069.500 [Categoria DeCS]
Referências encontradas : 449 [refinar]
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[PMID]:28603917
[Au] Autor:Sackmann Sala L; Boutillon F; Menara G; De Goyon-Pélard A; Leprévost M; Codzamanian J; Lister N; Pencik J; Clark A; Cagnard N; Bole-Feysot C; Moriggl R; Risbridger GP; Taylor RA; Kenner L; Guidotti JE; Goffin V
[Ad] Endereço:Institut Necker Enfants Malades (INEM), Inserm U1151-CNRS UMR 8253, University Paris Descartes, Sorbonne Paris Cité, Faculty of Medicine, Paris, France.
[Ti] Título:A rare castration-resistant progenitor cell population is highly enriched in Pten-null prostate tumours.
[So] Source:J Pathol;243(1):51-64, 2017 Sep.
[Is] ISSN:1096-9896
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Castration-resistant prostate cancer is a lethal disease. The cell type(s) that survive androgen deprivation remain poorly described, despite global efforts to understand the various mechanisms of therapy resistance. We recently identified in wild-type (WT) mouse prostates a rare population of luminal progenitor cells that we called LSC according to their FACS profile (Lin /Sca-1 /CD49f ). Here, we investigated the prevalence and castration resistance of LSC in various mouse models of prostate tumourigenesis (Pb-PRL, Pten , and Hi-Myc mice). LSC prevalence is low (∼8%, similar to WT) in Hi-Myc mice, where prostatic androgen receptor signalling is unaltered, but is significantly higher in the two other models, where androgen receptor signalling is decreased, rising up to more than 80% in Pten prostates. LSC tolerate androgen deprivation and persist or are enriched 2-3 weeks after castration. The tumour-initiating properties of LSC from Pten mice were demonstrated by regeneration of tumours in vivo. Transcriptomic analysis revealed that LSC represent a unique cell entity as their gene expression profile is different from luminal and basal/stem cells, but shares markers of each. Their intrinsic androgen signalling is markedly decreased, explaining why LSC tolerate androgen deprivation. This also illuminates why Pten tumours are castration-resistant since LSC represent the most prevalent cell type in this model. We validated CK4 as a specific marker for LSC on sorted cells and prostate tissues by immunostaining, allowing for the detection of LSC in various mouse prostate specimens. In castrated Pten prostates, there was significant proliferation of CK4 cells, further demonstrating their key role in castration-resistant prostate cancer progression. Taken together, this study identifies LSC as a probable source of prostate cancer relapse after androgen deprivation and as a new therapeutic target for the prevention of castrate-resistant prostate cancer. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/deficiência
Proliferação Celular
Células-Tronco Neoplásicas/enzimologia
PTEN Fosfo-Hidrolase/deficiência
Neoplasias de Próstata Resistentes à Castração/enzimologia
[Mh] Termos MeSH secundário: Antagonistas de Androgênios/farmacologia
Animais
Antineoplásicos Hormonais/farmacologia
Ataxina-1/metabolismo
Biomarcadores Tumorais/genética
Linhagem da Célula
Proliferação Celular/efeitos dos fármacos
Resistência a Medicamentos Antineoplásicos
Perfilação da Expressão Gênica/métodos
Regulação Neoplásica da Expressão Gênica
Predisposição Genética para Doença
Integrina alfa6/metabolismo
Queratina-4/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Recidiva Local de Neoplasia
Células-Tronco Neoplásicas/efeitos dos fármacos
Células-Tronco Neoplásicas/patologia
Células-Tronco Neoplásicas/transplante
Análise de Sequência com Séries de Oligonucleotídeos
PTEN Fosfo-Hidrolase/genética
Fenótipo
Neoplasias de Próstata Resistentes à Castração/tratamento farmacológico
Neoplasias de Próstata Resistentes à Castração/genética
Neoplasias de Próstata Resistentes à Castração/patologia
Receptores Androgênicos/efeitos dos fármacos
Receptores Androgênicos/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AR protein, mouse); 0 (Androgen Antagonists); 0 (Antineoplastic Agents, Hormonal); 0 (Ataxin-1); 0 (Atxn1 protein, mouse); 0 (Biomarkers, Tumor); 0 (Integrin alpha6); 0 (Keratin-4); 0 (Receptors, Androgen); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (Pten protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE
[do] DOI:10.1002/path.4924


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[PMID]:28288114
[Au] Autor:Lu HC; Tan Q; Rousseaux MW; Wang W; Kim JY; Richman R; Wan YW; Yeh SY; Patel JM; Liu X; Lin T; Lee Y; Fryer JD; Han J; Chahrour M; Finnell RH; Lei Y; Zurita-Jimenez ME; Ahimaz P; Anyane-Yeboa K; Van Maldergem L; Lehalle D; Jean-Marcais N; Mosca-Boidron AL; Thevenon J; Cousin MA; Bro DE; Lanpher BC; Klee EW; Alexander N; Bainbridge MN; Orr HT; Sillitoe RV; Ljungberg MC; Liu Z; Schaaf CP; Zoghbi HY
[Ad] Endereço:Program in Developmental Biology, Baylor College of Medicine, Houston, Texas, USA.
[Ti] Título:Disruption of the ATXN1-CIC complex causes a spectrum of neurobehavioral phenotypes in mice and humans.
[So] Source:Nat Genet;49(4):527-536, 2017 Apr.
[Is] ISSN:1546-1718
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gain-of-function mutations in some genes underlie neurodegenerative conditions, whereas loss-of-function mutations in the same genes have distinct phenotypes. This appears to be the case with the protein ataxin 1 (ATXN1), which forms a transcriptional repressor complex with capicua (CIC). Gain of function of the complex leads to neurodegeneration, but ATXN1-CIC is also essential for survival. We set out to understand the functions of the ATXN1-CIC complex in the developing forebrain and found that losing this complex results in hyperactivity, impaired learning and memory, and abnormal maturation and maintenance of upper-layer cortical neurons. We also found that CIC activity in the hypothalamus and medial amygdala modulates social interactions. Informed by these neurobehavioral features in mouse mutants, we identified five individuals with de novo heterozygous truncating mutations in CIC who share similar clinical features, including intellectual disability, attention deficit/hyperactivity disorder (ADHD), and autism spectrum disorder. Our study demonstrates that loss of ATXN1-CIC complexes causes a spectrum of neurobehavioral phenotypes.
[Mh] Termos MeSH primário: Ataxina-1/genética
Transtorno do Espectro Autista/genética
Doenças Neurodegenerativas/genética
Proteínas Nucleares/genética
Proteínas Repressoras/genética
[Mh] Termos MeSH secundário: Animais
Cerebelo/patologia
Feminino
Seres Humanos
Deficiência Intelectual/genética
Relações Interpessoais
Masculino
Camundongos
Proteínas do Tecido Nervoso/genética
Fenótipo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ataxin-1); 0 (Nerve Tissue Proteins); 0 (Nuclear Proteins); 0 (Repressor Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171001
[Lr] Data última revisão:
171001
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170314
[St] Status:MEDLINE
[do] DOI:10.1038/ng.3808


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[PMID]:28212558
[Au] Autor:Kang AR; An HT; Ko J; Kang S
[Ad] Endereço:Division of Life Sciences, College of Life Sciences and Biotechnology, Korea University, Seoul 02841, Korea.
[Ti] Título:Ataxin-1 regulates epithelial-mesenchymal transition of cervical cancer cells.
[So] Source:Oncotarget;8(11):18248-18259, 2017 Mar 14.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The mutant form of the protein ataxin-1 (ATXN1) causes the neurodegenerative disease spinocerebellar ataxia type-1. Recently, ATXN1 was reported to enhance E-cadherin expression in the breast cancer cell line MCF-7, suggesting a potential association between ATXN1 and cancer development. In the present study, we discovered a novel mechanism through which ATXN1 regulates the epithelial-mesenchymal transition (EMT) of cancer cells. Hypoxia-induced upregulation of the Notch intracellular domain expression decreased ATXN1 expression via MDM2-associated ubiquitination and degradation. In cervical cancer cells, ATXN1 knockdown induced EMT by directly regulating Snail expression, leading to matrix metalloproteinase activation and the promotion of cell migration and invasion. These findings provide insights into a novel mechanism of tumorigenesis and will facilitate the development of new and more effective therapies for cancer.
[Mh] Termos MeSH primário: Ataxina-1/metabolismo
Neoplasias do Colo do Útero/metabolismo
Neoplasias do Colo do Útero/patologia
[Mh] Termos MeSH secundário: Ataxina-1/biossíntese
Ataxina-1/genética
Hipóxia Celular/fisiologia
Linhagem Celular Tumoral
Transição Epitelial-Mesenquimal
Feminino
Células HEK293
Células HeLa
Seres Humanos
Metaloproteinases da Matriz/metabolismo
Proteínas/metabolismo
Proteínas Proto-Oncogênicas c-mdm2/metabolismo
Transdução de Sinais
Fatores de Transcrição da Família Snail/biossíntese
Transfecção
Neoplasias do Colo do Útero/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATXN1 protein, human); 0 (Ataxin-1); 0 (CRCT1 protein, human); 0 (Proteins); 0 (Snail Family Transcription Factors); EC 2.3.2.27 (MDM2 protein, human); EC 2.3.2.27 (Proto-Oncogene Proteins c-mdm2); EC 3.4.24.- (Matrix Metalloproteinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170218
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15319


  4 / 449 MEDLINE  
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[PMID]:27856257
[Au] Autor:Yang P; Yang WW; Chen X; Kaushal S; Dong D; Shen WB
[Ad] Endereço:Department of Obstetrics, Gynecology & Reproductive Sciences, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
[Ti] Título:Maternal diabetes and high glucose in vitro trigger Sca1 cardiac progenitor cell apoptosis through FoxO3a.
[So] Source:Biochem Biophys Res Commun;482(4):575-581, 2017 Jan 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent controversies surrounding the authenticity of c-kit cardiac progenitor cells significantly push back the advance in regenerative therapies for cardiovascular diseases. There is an urgent need for research in characterizing alternative types of cardiac progenitor cells. Towards this goal, in the present study, we determined the effect of maternal diabetes on Sca1 cardiac progenitor cells. Maternal diabetes induced caspase 3-dependent apoptosis in Sca1 cardiac progenitor cells derived from embryonic day 17.5 (E17.5). Similarly, high glucose in vitro but not the glucose osmotic control mannitol triggered Sca1 cardiac progenitor cell apoptosis in a dose- and time-dependent manner. Both maternal diabetes and high glucose in vitro activated the pro-apoptotic transcription factor, Forkhead O 3a (FoxO3a) via dephosphorylation at threonine 32 (Thr-32) residue. foxo3a gene deletion abolished maternal diabetes-induced Sca1 cardiac progenitor cell apoptosis. The dominant negative FoxO3a mutant without the transactivation domain from the C terminus blocked high glucose-induced Sca1 cardiac progenitor cell apoptosis, whereas the constitutively active FoxO3a mutant with the three phosphorylation sites, Thr-32, Ser-253, and Ser-315, being replaced by alanine residues mimicked the pro-apoptotic effect of high glucose. Thus, maternal diabetes and high glucose in vitro may limit the regenerative potential of Sca1 cardiac progenitor cells by inducing apoptosis through FoxO3a activation. These findings will serve as the guide in optimizing the autologous therapy using Sca1 cardiac progenitor cells in cardiac defect babies born exposed to maternal diabetes.
[Mh] Termos MeSH primário: Ataxina-1/metabolismo
Caspase 3/metabolismo
Diabetes Gestacional/patologia
Proteína Forkhead Box O3/metabolismo
Glucose/metabolismo
Miocárdio/patologia
Células-Tronco/patologia
[Mh] Termos MeSH secundário: Animais
Apoptose
Diabetes Gestacional/genética
Diabetes Gestacional/metabolismo
Embrião de Mamíferos/citologia
Embrião de Mamíferos/patologia
Feminino
Proteína Forkhead Box O3/genética
Deleção de Genes
Coração/embriologia
Cardiopatias Congênitas/etiologia
Cardiopatias Congênitas/genética
Cardiopatias Congênitas/metabolismo
Cardiopatias Congênitas/patologia
Camundongos Endogâmicos C57BL
Miocárdio/citologia
Miocárdio/metabolismo
Gravidez
Células-Tronco/citologia
Células-Tronco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ataxin-1); 0 (Atxn1 protein, mouse); 0 (Forkhead Box Protein O3); 0 (FoxO3 protein, mouse); EC 3.4.22.- (Caspase 3); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170529
[Lr] Data última revisão:
170529
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161119
[St] Status:MEDLINE


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[PMID]:27847151
[Au] Autor:Wang XZ; Gao RL; Sun P; Liu S; Xu Y; Liang DZ; Yin LM; Phillips WD; Liang SX
[Ad] Endereço:Department of Clinical Laboratory, the First Affiliated Hospital of Jinzhou Medical University, Jinzhou 121001,China.
[Ti] Título:Proliferation, differentiation and migration of SCA1 /CD31 cardiac side population cells in vitro and in vivo.
[So] Source:Int J Cardiol;227:378-386, 2017 Jan 15.
[Is] ISSN:1874-1754
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Side-population (SP) cells, identified by their capacity to efflux Hoechst dye, are highly enriched for stem/progenitor cell activity. They are found in many mammalian tissues, including mouse heart. Studies suggest that cardiac SP (CSP) cells can be divided into SCA1 /CD31 , SCA1 /CD31 and SCA1 /CD31 CSP subpopulations. SCA1 /CD31 were shown to be cardiac and endothelial stem/progenitors while SCA1 /CD31 CSP cells are endothelial progenitors. SCA1 /CD31 CSP cells remain to be fully characterized. In this study, we characterized SCA1 /CD31 CSP cells in the adult mouse heart, and investigated their abilities to proliferate, differentiate and migrate in vitro and in vivo. METHODS AND RESULTS: Using fluorescence-activated cell sorting, reverse transcriptase/polymerase chain reaction, assays of cell proliferation, differentiation and migration, and a murine model of myocardial infarction we show that SCA1 /CD31 CSP cells are located in the heart mesenchyme and express genes characteristic of stem cells and endothelial progenitors. These cells were capable of proliferation, differentiation, migration and vascularization in vitro and in vivo. Following experimental myocardial infarction, the SCA1 /CD31 CSP cells migrated from non-infarcted areas to the infarcted region within the myocardium where they differentiated into endothelial cells forming vascular (tube-like) structures. We further demonstrated that the SDF-1α/CXCR4 pathway may play an important role in migration of these cells after myocardial infarction. CONCLUSIONS: Based on their gene expression profile, localization and ability to proliferate, differentiate, migrate and vascularize in vitro and in vivo, we conclude that SCA1 /CD31 CSP cells may serve as endothelial progenitor cells in the adult mouse heart.
[Mh] Termos MeSH primário: Ataxina-1/fisiologia
Células Endoteliais/fisiologia
Infarto do Miocárdio/patologia
Miócitos Cardíacos/fisiologia
Molécula-1 de Adesão Celular Endotelial de Plaquetas/fisiologia
Células da Side Population/fisiologia
[Mh] Termos MeSH secundário: Animais
Técnicas de Cultura de Células
Diferenciação Celular
Movimento Celular
Proliferação Celular
Modelos Animais de Doenças
Feminino
Camundongos
Camundongos Endogâmicos C57BL
Infarto do Miocárdio/etiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ataxin-1); 0 (Platelet Endothelial Cell Adhesion Molecule-1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161117
[St] Status:MEDLINE


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[PMID]:27306906
[Au] Autor:Cvetanovic M; Hu YS; Opal P
[Ad] Endereço:Department of Neuroscience, University of Minnesota, Minneapolis, MN, USA.
[Ti] Título:Mutant Ataxin-1 Inhibits Neural Progenitor Cell Proliferation in SCA1.
[So] Source:Cerebellum;16(2):340-347, 2017 Apr.
[Is] ISSN:1473-4230
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Spinocerebellar ataxia type 1 (SCA1) is a dominantly inherited neurodegenerative disease caused by the expansion of a polyglutamine (Q) repeat tract in the protein ataxin-1 (ATXN1). Beginning as a cerebellar ataxic disorder, SCA1 progresses to involve the cerebral cortex, hippocampus, and brainstem. Using SCA1 knock-in mice that mirror the complexity of the human disease, we report a significant decrease in the capacity of adult neuronal progenitor cells (NPCs) to proliferate. Remarkably, a decrease in NPCs proliferation can be observed in vitro, outside the degenerative milieu of surrounding neurons or glia, demonstrating that mutant ATXN1 acting cell autonomously within progenitor cells interferes with their ability to proliferate. Our findings suggest that compromised adult neurogenesis contributes to the progressive pathology of the disease particularly in areas such as the hippocampus and cerebral cortex where stem cells provide neurotropic factors and participate in adult neurogenesis. These findings not only shed light on the biology of the disease but also have therapeutic implications in any future stem cell-based clinical trials.
[Mh] Termos MeSH primário: Células-Tronco Adultas/metabolismo
Ataxina-1/metabolismo
Proliferação Celular/fisiologia
Células-Tronco Neurais/metabolismo
Neurogênese/fisiologia
Ataxias Espinocerebelares/metabolismo
[Mh] Termos MeSH secundário: Células-Tronco Adultas/patologia
Animais
Ataxina-1/genética
Western Blotting
Bromodesoxiuridina
Células Cultivadas
Modelos Animais de Doenças
Técnicas de Introdução de Genes
Imuno-Histoquímica
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Mutação
Células-Tronco Neurais/patologia
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Nicho de Células-Tronco/fisiologia
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ataxin-1); 0 (Vascular Endothelial Growth Factor A); 0 (vascular endothelial growth factor A, mouse); G34N38R2N1 (Bromodeoxyuridine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160617
[St] Status:MEDLINE
[do] DOI:10.1007/s12311-016-0794-9


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[PMID]:27802273
[Au] Autor:Huda F; Fan Y; Suzuki M; Konno A; Matsuzaki Y; Takahashi N; Chan JK; Hirai H
[Ad] Endereço:Department of Neurophysiology & Neural Repair, Gunma University Graduate School of Medicine, Maebashi, Gunma 371-8511, Japan.
[Ti] Título:Fusion of Human Fetal Mesenchymal Stem Cells with "Degenerating" Cerebellar Neurons in Spinocerebellar Ataxia Type 1 Model Mice.
[So] Source:PLoS One;11(11):e0164202, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mesenchymal stem cells (MSCs) migrate to damaged tissues, where they participate in tissue repair. Human fetal MSCs (hfMSCs), compared with adult MSCs, have higher proliferation rates, a greater differentiation capacity and longer telomeres with reduced senescence. Therefore, transplantation of quality controlled hfMSCs is a promising therapeutic intervention. Previous studies have shown that intravenous or intracortical injections of MSCs result in the emergence of binucleated cerebellar Purkinje cells (PCs) containing an MSC-derived marker protein in mice, thus suggesting a fusion event. However, transdifferentiation of MSCs into PCs or transfer of a marker protein from an MSC to a PC cannot be ruled out. In this study, we unequivocally demonstrated the fusion of hfMSCs with murine PCs through a tetracycline-regulated (Tet-off) system with or without a Cre-dependent genetic inversion switch (flip-excision; FLEx). In the FLEx-Tet system, we performed intra-cerebellar injection of viral vectors expressing tetracycline transactivator (tTA) and Cre recombinase into either non-symptomatic (4-week-old) or clearly symptomatic (6-8-month-old) spinocerebellar ataxia type 1 (SCA1) mice. Then, the mice received an injection of 50,000 genetically engineered hfMSCs that expressed GFP only in the presence of Cre recombinase and tTA. We observed a significant emergence of GFP-expressing PCs and interneurons in symptomatic, but not non-symptomatic, SCA1 mice 2 weeks after the MSC injection. These results, together with the results obtained using age-matched wild-type mice, led us to conclude that hfMSCs have the potential to preferentially fuse with degenerating PCs and interneurons but not with healthy neurons.
[Mh] Termos MeSH primário: Ataxina-1/metabolismo
Cerebelo/citologia
Feto/citologia
Células Mesenquimais Estromais/citologia
Neurônios/citologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/fisiologia
Transdiferenciação Celular/fisiologia
Cerebelo/metabolismo
Modelos Animais de Doenças
Células-Tronco Fetais/citologia
Células-Tronco Fetais/metabolismo
Feto/metabolismo
Seres Humanos
Transplante de Células-Tronco Mesenquimais/métodos
Células Mesenquimais Estromais/metabolismo
Camundongos
Camundongos Transgênicos
Neurônios/metabolismo
Células de Purkinje/citologia
Células de Purkinje/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ataxin-1); 0 (Atxn1 protein, mouse)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170621
[Lr] Data última revisão:
170621
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161102
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0164202


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[PMID]:27686464
[Au] Autor:Keiser MS; Monteys AM; Corbau R; Gonzalez-Alegre P; Davidson BL
[Ad] Endereço:Raymond G. Perelman Center for Cellular and Molecular Therapeutics, Children's Hospital of Philadelphia, Philadelphia, PA.
[Ti] Título:RNAi prevents and reverses phenotypes induced by mutant human ataxin-1.
[So] Source:Ann Neurol;80(5):754-765, 2016 Nov.
[Is] ISSN:1531-8249
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Spinocerebellar ataxia type 1 is an autosomal dominant fatal neurodegenerative disease caused by a polyglutamine expansion in the coding region of ATXN1. We showed previously that partial suppression of mutant ataxin-1 (ATXN1) expression, using virally expressed RNAi triggers, could prevent disease symptoms in a transgenic mouse model and a knockin mouse model of the disease, using a single dose of virus. Here, we set out to test whether RNAi triggers targeting ATXN1 could not only prevent, but also reverse disease readouts when delivered after symptom onset. METHODS: We administered recombinant adeno-associated virus (rAAV) expressing miS1, an artificial miRNA targeting human ATXN1 mRNA (rAAV.miS1), to a mouse model of spinocerebellar ataxia type 1 (SCA1; B05 mice). Viruses were delivered prior to or after symptom onset at multiple doses. Control B05 mice were treated with rAAVs expressing a control artificial miRNA, or with saline. Animal behavior, molecular phenotypes, neuropathology, and magnetic resonance spectroscopy were done on all groups, and data were compared to wild-type littermates. RESULTS: We found that SCA1 phenotypes could be reversed by partial suppression of human mutant ATXN1 mRNA by rAAV.miS1 when delivered after symptom onset. We also identified the therapeutic range of rAAV.miS1 that could prevent or reverse disease readouts. INTERPRETATION: SCA1 disease may be reversible by RNAi therapy, and the doses required for advancing this therapy to humans are delineated. Ann Neurol 2016;80:754-765.
[Mh] Termos MeSH primário: Ataxina-1/metabolismo
Terapia Genética/métodos
Vetores Genéticos
Interferência de RNA
Ataxias Espinocerebelares/fisiopatologia
Ataxias Espinocerebelares/terapia
[Mh] Termos MeSH secundário: Animais
Comportamento Animal
Dependovirus
Modelos Animais de Doenças
Células HEK293
Seres Humanos
Camundongos
Camundongos Transgênicos
Fenótipo
RNA Mensageiro
Ataxias Espinocerebelares/prevenção & controle
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATXN1 protein, human); 0 (Ataxin-1); 0 (RNA, Messenger)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161001
[St] Status:MEDLINE
[do] DOI:10.1002/ana.24789


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[PMID]:27618218
[Au] Autor:Kramann R; Goettsch C; Wongboonsin J; Iwata H; Schneider RK; Kuppe C; Kaesler N; Chang-Panesso M; Machado FG; Gratwohl S; Madhurima K; Hutcheson JD; Jain S; Aikawa E; Humphreys BD
[Ad] Endereço:Division of Nephrology and Clinical Immunology, Medical Faculty RWTH Aachen University, RWTH Aachen University, 52074 Aachen, Germany; Renal Division, Brigham and Women's Hospital and Department of Medicine, Harvard Medical School, Boston, MA 02138, USA. Electronic address: rkramann@gmx.net.
[Ti] Título:Adventitial MSC-like Cells Are Progenitors of Vascular Smooth Muscle Cells and Drive Vascular Calcification in Chronic Kidney Disease.
[So] Source:Cell Stem Cell;19(5):628-642, 2016 Nov 03.
[Is] ISSN:1875-9777
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mesenchymal stem cell (MSC)-like cells reside in the vascular wall, but their role in vascular regeneration and disease is poorly understood. Here, we show that Gli1 cells located in the arterial adventitia are progenitors of vascular smooth muscle cells and contribute to neointima formation and repair after acute injury to the femoral artery. Genetic fate tracing indicates that adventitial Gli1 MSC-like cells migrate into the media and neointima during athero- and arteriosclerosis in ApoE mice with chronic kidney disease. Our data indicate that Gli1 cells are a major source of osteoblast-like cells during calcification in the media and intima. Genetic ablation of Gli1 cells before induction of kidney injury dramatically reduced the severity of vascular calcification. These findings implicate Gli1 cells as critical adventitial progenitors in vascular remodeling after acute and during chronic injury and suggest that they may be relevant therapeutic targets for mitigation of vascular calcification.
[Mh] Termos MeSH primário: Túnica Adventícia/patologia
Células Mesenquimais Estromais/patologia
Músculo Liso Vascular/patologia
Miócitos de Músculo Liso/patologia
Insuficiência Renal Crônica/complicações
Células-Tronco/patologia
Calcificação Vascular/complicações
[Mh] Termos MeSH secundário: Idoso
Animais
Antígenos CD34/metabolismo
Ataxina-1/metabolismo
Biomarcadores/metabolismo
Desdiferenciação Celular
Diferenciação Celular
Linhagem da Célula
Movimento Celular
Proliferação Celular
Feminino
Proteínas Hedgehog/metabolismo
Seres Humanos
Masculino
Células Mesenquimais Estromais/metabolismo
Camundongos Transgênicos
Miócitos de Músculo Liso/metabolismo
Neointima/patologia
Osteoblastos/metabolismo
Osteoblastos/patologia
Placa Aterosclerótica/patologia
Receptor beta de Fator de Crescimento Derivado de Plaquetas/metabolismo
Insuficiência Renal Crônica/patologia
Calcificação Vascular/patologia
Remodelação Vascular
Proteína GLI1 em Dedos de Zinco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD34); 0 (Ataxin-1); 0 (Biomarkers); 0 (GLI1 protein, human); 0 (Gli protein, mouse); 0 (Hedgehog Proteins); 0 (SHH protein, human); 0 (Zinc Finger Protein GLI1); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor beta)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160913
[St] Status:MEDLINE


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[PMID]:27577232
[Au] Autor:Tian S; Zhao Q; Yang X; An R; Xu Y
[Ad] Endereço:Department of Neurology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China. Email: neuroxym@163.com.
[Ti] Título:[Spinocerebellar ataxia: eight cases from one pedigree].
[So] Source:Zhonghua Yi Xue Yi Chuan Xue Za Zhi;33(5):726-7, 2016 Oct.
[Is] ISSN:1003-9406
[Cp] País de publicação:China
[La] Idioma:chi
[Mh] Termos MeSH primário: Ataxina-1/genética
Ataxias Espinocerebelares/genética
Expansão das Repetições de Trinucleotídeos/genética
[Mh] Termos MeSH secundário: Adulto
Análise Mutacional de DNA
Saúde da Família
Feminino
Seres Humanos
Masculino
Meia-Idade
Linhagem
Ataxias Espinocerebelares/diagnóstico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ataxin-1)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170105
[Lr] Data última revisão:
170105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160901
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1003-9406.2016.05.034



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