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Pesquisa : D12.776.260.103.798 [Categoria DeCS]
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[PMID]:28521040
[Au] Autor:Strijbis EMM; Kooi EJ; van der Valk P; Geurts JJG
[Ad] Endereço:From the Department of Neurology (EMMS), Department of Anatomy & Neurosciences, Section of Clinical Neuroscience (EMMS, E-JK, JJGG), VU University Medical Center, De Boelelaan 1118, 1081 HV Amsterdam, The Netherlands; and Department of Pathology (Neuropathology), VU University Medical Center, De
[Ti] Título:Cortical Remyelination Is Heterogeneous in Multiple Sclerosis.
[So] Source:J Neuropathol Exp Neurol;76(5):390-401, 2017 05 01.
[Is] ISSN:1554-6578
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cortical lesions (CLs) are an important component of multiple sclerosis (MS) pathology; they correlate better with physical disability and cognitive impairment than white matter lesions (WMLs). Because remyelination can be extensive in CLs, we quantified remyelination in gray matter (GM) and white matter (WM), addressing oligodendrocyte (OGD) maturation state and clinical relevance of remyelination. Brain tissue samples from 21 chronic MS patients were immunohistochemically stained for myelin proteolipid protein, Olig2, which is strongly expressed in OGD precursor cells (OPCs), but weakly expressed in mature OGDs and other OGD markers. Sections were scored for the presence of normal-appearing WM and GM, de- and remyelination, and OPC and OGD cell counts. Remyelination was significantly more extensive in CLs than in WMLs with a trend toward more GM remyelination in primary progressive MS (PPMS) vs relapse-onset MS patients. More OPCs were found in remyelinated and nonremyelinated CLs vs remyelinated WMLs and nonremyelinated WMLs. Thus, there is more remyelination in the GM than in the WM in MS patient brains, with a trend toward more remyelination in those with PPMS. There does not seem to be a significant OPC recruitment failure in the GM, which casts new light on the process of remyelination failure.
[Mh] Termos MeSH primário: Córtex Cerebral/patologia
Esclerose Múltipla/patologia
Bainha de Mielina/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo
Contagem de Células
Doenças Desmielinizantes/patologia
Feminino
Substância Cinzenta/patologia
Seres Humanos
Imuno-Histoquímica
Masculino
Meia-Idade
Proteínas do Tecido Nervoso/metabolismo
Células-Tronco Neurais/patologia
Fator de Transcrição 2 de Oligodendrócitos
Oligodendroglia/patologia
Substância Branca/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Nerve Tissue Proteins); 0 (OLIG2 protein, human); 0 (Oligodendrocyte Transcription Factor 2)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.1093/jnen/nlx023


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[PMID]:28423639
[Au] Autor:Yuan J; Ge H; Liu W; Zhu H; Chen Y; Zhang X; Yang Y; Yin Y; Chen W; Wu W; Yang Y; Lin J
[Ad] Endereço:Department of Neurosurgery and Key Laboratory of Neurotrauma, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.
[Ti] Título:M2 microglia promotes neurogenesis and oligodendrogenesis from neural stem/progenitor cells via the PPARγ signaling pathway.
[So] Source:Oncotarget;8(12):19855-19865, 2017 Mar 21.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neural stem/progenitor cells (NSPCs) are an important source of cells for cell replacement therapy after nerve injury. How to induce NSPCs differentiation towards neurons and oligodendrocytes is a challenging issue in neuroscience research. In the present study, we polarized microglia into M1 and M2 phenotype, used their supernatants to induce NSPCs differentiation, and investigated the effects of different microglia phenotypes on NSPCs differentiation and their mechanisms. We discovered that, after exposure to M1 phenotype supernatant, NSPCs differentiated into fewer Tuj-1+ and Olig2+ cells, but more GFAP+ cells. Meanwhile, a significantly increased number of Tuj-1+ and Olig2+ cells and smaller number of GFAP+ cells were generated by M2 microglia supernatant-induced NSPCs differentiation. We also observed that 15d-PGJ2, an endogenous ligand of PPARγ, was elevated in M2 phenotype supernatant and could activate PPARγ expression in NSPCs, whereas use of the PPARγ inhibitor GW9662, could reduce the percentage of differentiated neurons and oligodendrocytes. Our study results confirm that M2 microglia supernatant can activate the PPARγ signaling pathway and promote neurogenesis and oligodendrogenesis from NSPCs differentiation. The present study provides a further theoretical basis for induction of NSPCs oriented differentiation.
[Mh] Termos MeSH primário: Microglia/metabolismo
Células-Tronco Neurais/fisiologia
Oligodendroglia/fisiologia
PPAR gama/metabolismo
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Anilidas/farmacologia
Animais
Animais Recém-Nascidos
Apoptose/efeitos dos fármacos
Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo
Western Blotting
Diferenciação Celular/efeitos dos fármacos
Polaridade Celular
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Meios de Cultivo Condicionados/metabolismo
Meios de Cultivo Condicionados/farmacologia
Proteína Glial Fibrilar Ácida/metabolismo
Camundongos Endogâmicos ICR
Microglia/classificação
Microglia/citologia
Microscopia de Fluorescência
Proteínas do Tecido Nervoso/metabolismo
Células-Tronco Neurais/citologia
Neurogênese/efeitos dos fármacos
Neurogênese/fisiologia
Fator de Transcrição 2 de Oligodendrócitos
Oligodendroglia/citologia
PPAR gama/agonistas
PPAR gama/antagonistas & inibidores
Prostaglandina D2/análogos & derivados
Prostaglandina D2/metabolismo
Prostaglandina D2/farmacologia
Transdução de Sinais/efeitos dos fármacos
Tubulina (Proteína)/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (15-deoxyprostaglandin J2); 0 (2-chloro-5-nitrobenzanilide); 0 (Anilides); 0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Culture Media, Conditioned); 0 (Glial Fibrillary Acidic Protein); 0 (Nerve Tissue Proteins); 0 (OLIG2 protein, human); 0 (Oligodendrocyte Transcription Factor 2); 0 (PPAR gamma); 0 (TUBB3 protein, human); 0 (Tubulin); RXY07S6CZ2 (Prostaglandin D2)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170421
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15774


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[PMID]:28351411
[Au] Autor:Albrecht S; Fleck AK; Kirchberg I; Hucke S; Liebmann M; Klotz L; Kuhlmann T
[Ad] Endereço:Institute of Neuropathology, University Hospital Münster, 48149, Münster, Germany.
[Ti] Título:Activation of FXR pathway does not alter glial cell function.
[So] Source:J Neuroinflammation;14(1):66, 2017 Mar 28.
[Is] ISSN:1742-2094
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The nuclear receptor farnesoid-X-receptor (FXR; NR1H4) is expressed not only in the liver, gut, kidney and adipose tissue but also in the immune cells. FXR has been shown to confer protection in several animal models of inflammation, including experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). FXR agonists are currently tested in clinical trials for treatment of human metabolic diseases. The beneficial effect of FXR agonists in EAE suggests that FXR might represent a potential target in inflammatory-demyelinating CNS diseases, such as MS. In MS, oligodendrocytes not only undergo cell death but also contribute to remyelination. This repair mechanism is impaired due to a differentiation block of oligodendroglial progenitor cells. Activation of other nuclear receptors that heterodimerize with FXR promote oligodendroglial differentiation. Therefore, we wanted to address the functional relevance of FXR for glial cells, especially for oligodendroglial differentiation. METHODS: We isolated primary murine oligodendrocytes from FXR-deficient (FXR Ko) and wild-type (WT) mice and determined the effect of FXR deficiency and activation on oligodendroglial differentiation by analysing markers of oligodendroglial progenitor cells (OPCs) and mature oligodendrocytes (OLs) using qRT-PCR and immunocytochemistry. Additionally, we determined whether FXR activation modulates the pro-inflammatory profile of astrocytes or microglia and whether this may subsequently modulate oligodendroglial differentiation. These in vitro studies were complemented by histological analyses of oligodendrocytes in FXR Ko mice. RESULTS: FXR is expressed by OPCs and mature oligodendrocytes. However, lack of FXR did not affect oligodendroglial differentiation in vitro or in vivo. Furthermore, activation of FXR using the synthetic agonist GW4064 did not affect oligodendroglial differentiation, remyelination in an ex vivo model or the expression of pro-inflammatory molecules in astrocytes or microglia. Concordantly, no effects of supernatants from macrophages cultured in the presence of GW4064 were observed regarding a possible indirect impact on oligodendroglial differentiation. CONCLUSIONS: Our data suggest that FXR is dispensable for oligodendroglial differentiation and that FXR agonists, such as GW4064, represent a potential therapeutic approach for MS which specifically targets peripheral immune cells including macrophages but not brain-resident cells, such as oligodendrocytes, astrocytes or microglia.
[Mh] Termos MeSH primário: Oligodendroglia/metabolismo
Receptores Citoplasmáticos e Nucleares/metabolismo
[Mh] Termos MeSH secundário: Animais
Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo
Células Cultivadas
Cerebelo/citologia
Citocinas/genética
Citocinas/metabolismo
Relação Dose-Resposta a Droga
Técnicas In Vitro
Isoxazóis/farmacologia
Macrófagos/efeitos dos fármacos
Macrófagos/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Proteína Básica da Mielina/genética
Proteína Básica da Mielina/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Óxido Nítrico/metabolismo
Proteínas Nogo/metabolismo
Fator de Transcrição 2 de Oligodendrócitos
Oligodendroglia/efeitos dos fármacos
RNA Mensageiro/metabolismo
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/genética
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/metabolismo
Receptores Citoplasmáticos e Nucleares/genética
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Cytokines); 0 (Isoxazoles); 0 (Myelin Basic Protein); 0 (Nerve Tissue Proteins); 0 (Nogo Proteins); 0 (Olig2 protein, mouse); 0 (Oligodendrocyte Transcription Factor 2); 0 (RNA, Messenger); 0 (Receptors, Cytoplasmic and Nuclear); 0 (Tumor Necrosis Factor-alpha); 0 (farnesoid X-activated receptor); 31C4KY9ESH (Nitric Oxide); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor alpha); SR225WUZ0H (GW 4064)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170330
[St] Status:MEDLINE
[do] DOI:10.1186/s12974-017-0833-6


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[PMID]:28328117
[Au] Autor:Siegfried A; Cances C; Denuelle M; Loukh N; Tauber M; Cavé H; Delisle MB
[Ad] Endereço:Department of Pathology, Institut Universitaire du Cancer, Oncopole, Toulouse, France.
[Ti] Título:Noonan syndrome, PTPN11 mutations, and brain tumors. A clinical report and review of the literature.
[So] Source:Am J Med Genet A;173(4):1061-1065, 2017 Apr.
[Is] ISSN:1552-4833
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Noonan syndrome (NS), an autosomal dominant disorder, is characterized by short stature, congenital heart defects, developmental delay, and facial dysmorphism. PTPN11 mutations are the most common cause of NS. PTPN11 encodes a non-receptor protein tyrosine phosphatase, SHP2. Hematopoietic malignancies and solid tumors are associated with NS. Among solid tumors, brain tumors have been described in children and young adults but remain rather rare. We report a 16-year-old boy with PTPN11-related NS who, at the age of 12, was incidentally found to have a left temporal lobe brain tumor and a cystic lesion in the right thalamus. He developed epilepsy 2 years later. The temporal tumor was surgically resected because of increasing crises and worsening radiological signs. Microscopy showed nodules with specific glioneuronal elements or glial nodules, leading to the diagnosis of dysembryoplastic neuroepithelial tumor (DNT). Immunohistochemistry revealed positive nuclear staining with Olig2 and pERK in small cells. SHP2 plays a key role in RAS/MAPK pathway signaling which controls several developmental cell processes and oncogenesis. An amino-acid substitution in the N-terminal SHP2 domain disrupts the self-locking conformation and leads to ERK activation. Glioneuronal tumors including DNTs and pilocytic astrocytomas have been described in NS. This report provides further support for the relation of DNTs with RASopathies and for the implication of RAS/MAPK pathways in sporadic low-grade glial tumors including DNTs. © 2017 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/genética
Epilepsia/genética
Mutação
Neoplasias Neuroepiteliomatosas/genética
Síndrome de Noonan/genética
Proteína Tirosina Fosfatase não Receptora Tipo 11/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo
Neoplasias Encefálicas/diagnóstico
Neoplasias Encefálicas/patologia
Neoplasias Encefálicas/cirurgia
Criança
Epilepsia/diagnóstico
Epilepsia/patologia
Epilepsia/cirurgia
MAP Quinases Reguladas por Sinal Extracelular/genética
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Expressão Gênica
Genes Dominantes
Seres Humanos
Masculino
Neoplasias Neuroepiteliomatosas/diagnóstico
Neoplasias Neuroepiteliomatosas/patologia
Neoplasias Neuroepiteliomatosas/cirurgia
Proteínas do Tecido Nervoso/genética
Proteínas do Tecido Nervoso/metabolismo
Síndrome de Noonan/diagnóstico
Síndrome de Noonan/patologia
Síndrome de Noonan/cirurgia
Fator de Transcrição 2 de Oligodendrócitos
Proteína Tirosina Fosfatase não Receptora Tipo 11/metabolismo
Lobo Temporal/metabolismo
Lobo Temporal/patologia
Lobo Temporal/cirurgia
Tálamo/metabolismo
Tálamo/patologia
Tálamo/cirurgia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Nerve Tissue Proteins); 0 (OLIG2 protein, human); 0 (Oligodendrocyte Transcription Factor 2); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 3.1.3.48 (PTPN11 protein, human); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 11)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170323
[St] Status:MEDLINE
[do] DOI:10.1002/ajmg.a.38108


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[PMID]:28241049
[Au] Autor:Brown DV; Filiz G; Daniel PM; Hollande F; Dworkin S; Amiridis S; Kountouri N; Ng W; Morokoff AP; Mantamadiotis T
[Ad] Endereço:Department of Pathology, University of Melbourne, Melbourne, Victoria, Australia.
[Ti] Título:Expression of CD133 and CD44 in glioblastoma stem cells correlates with cell proliferation, phenotype stability and intra-tumor heterogeneity.
[So] Source:PLoS One;12(2):e0172791, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glioblastoma (GBM) is a heterogeneous tumor of the brain with a poor prognosis due to recurrence and drug resistance following therapy. Genome-wide profiling has revealed the existence of distinct GBM molecular subtypes that respond differently to aggressive therapies. Despite this, molecular subtype does not predict recurrence or drug resistance and overall survival is similar across subtypes. One of the key features contributing to tumor recurrence and resistance to therapy is proposed to be an underlying subpopulation of resistant glioma stem cells (GSC). CD133 expression has been used as a marker of GSCs, however recent evidence suggests the relationship between CD133 expression, GSCs and molecular subtype is more complex than initially proposed. The expression of CD133, Olig2 and CD44 was investigated using patient derived glioma stem-like cells (PDGCs) in vitro and in vivo. Different PDGCs exhibited a characteristic equilibrium of distinct CD133+ and CD44+ subpopulations and the influence of environmental factors on the intra-tumor equilibrium of CD133+ and CD44+ cells in PDGCs was also investigated, with hypoxia inducing a CD44+ to CD133+ shift and chemo-radiotherapy inducing a CD133+ to CD44+ shift. These data suggest that surveillance and modulation of intra-tumor heterogeneity using molecular markers at initial surgery and surgery for recurrent GBM may be important for more effective management of GBM.
[Mh] Termos MeSH primário: Antígeno AC133/metabolismo
Neoplasias Encefálicas/metabolismo
Glioblastoma/metabolismo
Receptores de Hialuronatos/metabolismo
Células-Tronco Neoplásicas/metabolismo
[Mh] Termos MeSH secundário: Animais
Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo
Biomarcadores Tumorais/metabolismo
Neoplasias Encefálicas/patologia
Proliferação Celular
Feminino
Glioblastoma/patologia
Seres Humanos
Hipóxia
Camundongos
Camundongos Endogâmicos BALB C
Recidiva Local de Neoplasia
Células-Tronco Neoplásicas/patologia
Proteínas do Tecido Nervoso/metabolismo
Fator de Transcrição 2 de Oligodendrócitos
Fenótipo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AC133 Antigen); 0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Biomarkers, Tumor); 0 (CD44 protein, human); 0 (Hyaluronan Receptors); 0 (Nerve Tissue Proteins); 0 (OLIG2 protein, human); 0 (Oligodendrocyte Transcription Factor 2)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170228
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0172791


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[PMID]:28163160
[Au] Autor:Lyczek A; Arnold A; Zhang J; Campanelli JT; Janowski M; Bulte JW; Walczak P
[Ad] Endereço:Russell H. Morgan Dept. of Radiology and Radiological Science, Johns Hopkins University, Baltimore, MD, United States; Cellular Imaging Section and Vascular Biology Program, Institute for Cell Engineering, Johns Hopkins University, Baltimore, MD 21205, United States.
[Ti] Título:Transplanted human glial-restricted progenitors can rescue the survival of dysmyelinated mice independent of the production of mature, compact myelin.
[So] Source:Exp Neurol;291:74-86, 2017 May.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The therapeutic effect of glial progenitor transplantation in diseases of dysmyelination is currently attributed to the formation of new myelin. Using magnetic resonance imaging (MRI), we show that the therapeutic outcome in dysmyelinated shiverer mice is dependent on the extent of cell migration but not the presence of mature and compact myelin. Human or mouse glial restricted progenitors (GRPs) were transplanted into rag2 shiverer mouse neonates and followed for over one year. Mouse GRPs produced mature myelin as detected with multi-parametric MRI, but showed limited migration without extended animal lifespan. In sharp contrast, human GRPs migrated extensively and significantly increased animal survival, but production of mature myelin did not occur until 46weeks post-grafting. We conclude that human GRPs can extend the survival of transplanted shiverer mice prior to production of mature myelin, while mouse GRPs fail to extend animal survival despite the early presence of mature myelin. This paradox suggests that transplanted GRPs provide therapeutic benefits through biological processes other than the formation of mature myelin capable to foster rapid nerve conduction, challenging the current dogma of the primary role of myelination in regaining function of the central nervous system.
[Mh] Termos MeSH primário: Doenças Desmielinizantes/cirurgia
Bainha de Mielina/metabolismo
Neuroglia/transplante
Transplante de Células-Tronco
[Mh] Termos MeSH secundário: Animais
Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo
Encéfalo/diagnóstico por imagem
Diferenciação Celular
Movimento Celular
Sobrevivência Celular/genética
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Doenças Desmielinizantes/diagnóstico por imagem
Doenças Desmielinizantes/patologia
Modelos Animais de Doenças
Gangliosídeos/metabolismo
Proteína Glial Fibrilar Ácida/metabolismo
Seres Humanos
Camundongos
Camundongos Transgênicos
Proteína Básica da Mielina/metabolismo
Proteína Proteolipídica de Mielina/genética
Proteína Proteolipídica de Mielina/metabolismo
Bainha de Mielina/ultraestrutura
Proteínas do Tecido Nervoso/metabolismo
Neuroglia/fisiologia
Neuroglia/ultraestrutura
Fator de Transcrição 2 de Oligodendrócitos
Medula Espinal/diagnóstico por imagem
Fatores de Tempo
Tubulina (Proteína)/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (DNA-Binding Proteins); 0 (Gangliosides); 0 (Glial Fibrillary Acidic Protein); 0 (Mbp protein, mouse); 0 (Myelin Basic Protein); 0 (Myelin Proteolipid Protein); 0 (Nerve Tissue Proteins); 0 (Olig2 protein, mouse); 0 (Oligodendrocyte Transcription Factor 2); 0 (Plp1 protein, mouse); 0 (Rag2 protein, mouse); 0 (Tubulin); 0 (beta3 tubulin, mouse); 0 (ganglioside A2B5)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170207
[St] Status:MEDLINE


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[PMID]:28096221
[Au] Autor:Bressan RB; Dewari PS; Kalantzaki M; Gangoso E; Matjusaitis M; Garcia-Diaz C; Blin C; Grant V; Bulstrode H; Gogolok S; Skarnes WC; Pollard SM
[Ad] Endereço:MRC Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK.
[Ti] Título:Efficient CRISPR/Cas9-assisted gene targeting enables rapid and precise genetic manipulation of mammalian neural stem cells.
[So] Source:Development;144(4):635-648, 2017 02 15.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mammalian neural stem cell (NSC) lines provide a tractable model for discovery across stem cell and developmental biology, regenerative medicine and neuroscience. They can be derived from foetal or adult germinal tissues and continuously propagated as adherent monolayers. NSCs are clonally expandable, genetically stable, and easily transfectable - experimental attributes compatible with targeted genetic manipulations. However, gene targeting, which is crucial for functional studies of embryonic stem cells, has not been exploited to date in NSC lines. Here, we deploy CRISPR/Cas9 technology to demonstrate a variety of sophisticated genetic modifications via gene targeting in both mouse and human NSC lines, including: (1) efficient targeted transgene insertion at safe harbour loci ( and ); (2) biallelic knockout of neurodevelopmental transcription factor genes; (3) simple knock-in of epitope tags and fluorescent reporters (e.g. and ); and (4) engineering of glioma mutations ( deletion; point mutations). These resources and optimised methods enable facile and scalable genome editing in mammalian NSCs, providing significant new opportunities for functional genetic analysis.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/genética
Sistemas CRISPR-Cas
Marcação de Genes/métodos
Glioma/genética
Células-Tronco Neurais/citologia
[Mh] Termos MeSH secundário: Alelos
Animais
Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Neoplasias Encefálicas/metabolismo
Mapeamento de Epitopos
Epitopos
Glioma/metabolismo
Proteínas de Fluorescência Verde/metabolismo
Recombinação Homóloga
Seres Humanos
Camundongos
Camundongos Knockout
Mutação
Proteínas do Tecido Nervoso/genética
Fator de Transcrição 2 de Oligodendrócitos
Oligonucleotídeos/genética
Mutação Puntual
Recombinação Genética
Medicina Regenerativa
Transgenes
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Epitopes); 0 (Nerve Tissue Proteins); 0 (Olig2 protein, mouse); 0 (Oligodendrocyte Transcription Factor 2); 0 (Oligonucleotides); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170119
[St] Status:MEDLINE
[do] DOI:10.1242/dev.140855


  8 / 477 MEDLINE  
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[PMID]:27923998
[Au] Autor:Deng T; Postnikov Y; Zhang S; Garrett L; Becker L; Rácz I; Hölter SM; Wurst W; Fuchs H; Gailus-Durner V; de Angelis MH; Bustin M
[Ad] Endereço:Protein Section, Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
[Ti] Título:Interplay between H1 and HMGN epigenetically regulates OLIG1&2 expression and oligodendrocyte differentiation.
[So] Source:Nucleic Acids Res;45(6):3031-3045, 2017 Apr 07.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:An interplay between the nucleosome binding proteins H1 and HMGN is known to affect chromatin dynamics, but the biological significance of this interplay is still not clear. We find that during embryonic stem cell differentiation loss of HMGNs leads to down regulation of genes involved in neural differentiation, and that the transcription factor OLIG2 is a central node in the affected pathway. Loss of HMGNs affects the expression of OLIG2 as well as that of OLIG1, two transcription factors that are crucial for oligodendrocyte lineage specification and nerve myelination. Loss of HMGNs increases the chromatin binding of histone H1, thereby recruiting the histone methyltransferase EZH2 and elevating H3K27me3 levels, thus conferring a repressive epigenetic signature at Olig1&2 sites. Embryonic stem cells lacking HMGNs show reduced ability to differentiate towards the oligodendrocyte lineage, and mice lacking HMGNs show reduced oligodendrocyte count and decreased spinal cord myelination, and display related neurological phenotypes. Thus, the presence of HMGN proteins is required for proper expression of neural differentiation genes during embryonic stem cell differentiation. Specifically, we demonstrate that the dynamic interplay between HMGNs and H1 in chromatin epigenetically regulates the expression of OLIG1&2, thereby affecting oligodendrocyte development and myelination, and mouse behavior.
[Mh] Termos MeSH primário: Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Diferenciação Celular/genética
Epigênese Genética
Proteínas HMGN/fisiologia
Histonas/metabolismo
Proteínas do Tecido Nervoso/genética
Oligodendroglia/citologia
[Mh] Termos MeSH secundário: Animais
Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo
Linhagem Celular
Células-Tronco Embrionárias/metabolismo
Proteína Potenciadora do Homólogo 2 de Zeste/metabolismo
Feminino
Proteína HMGN1/genética
Proteína HMGN1/fisiologia
Proteína HMGN2/genética
Proteína HMGN2/fisiologia
Masculino
Camundongos
Camundongos Knockout
Proteínas do Tecido Nervoso/metabolismo
Fator de Transcrição 2 de Oligodendrócitos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (HMGN Proteins); 0 (HMGN1 Protein); 0 (HMGN2 Protein); 0 (Histones); 0 (Nerve Tissue Proteins); 0 (Olig1 protein, mouse); 0 (Olig2 protein, mouse); 0 (Oligodendrocyte Transcription Factor 2); EC 2.1.1.43 (Enhancer of Zeste Homolog 2 Protein); EC 2.1.1.43 (Ezh2 protein, mouse)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161208
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkw1222


  9 / 477 MEDLINE  
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[PMID]:27915062
[Au] Autor:Duan L; Zhang Y; Fu W; Geng S
[Ad] Endereço:Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China; China National Clinical Research Center for Neurological Diseases, Beijing, China.
[Ti] Título:Rosette-Forming Glioneuronal Tumor Originating From the Spinal Cord: Report of 2 Cases and Literature Review.
[So] Source:World Neurosurg;98:875.e1-875.e7, 2017 Feb.
[Is] ISSN:1878-8769
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rosette-forming glioneuronal tumor (RGNT) is a recently recognized and rarely encountered tumor occurring in the fourth ventricle. RGNT was first described as a new entity for the distinct clinicopathologic features by Komori et.al. in 2002. Histologically, it is composed of 2 distinct features: a glial component, resembling pilocytic astrocytoma, and a neurocytic component forming neurocytic rosettes and/or perivascular rosettes. We report 2 extremely rare cases of RGNT arising from the spinal cord, which were misdiagnosed as ependymoma and astrocytoma preoperatively. Symptoms included dissociated sensory disturbances and episodic pain and fatigue of 2 years' duration in case 1, as well as motor disturbance for 2 months' duration in case 2. Magnetic resonance imaging (MRI) revealed these masses in the thoracolumbar (T7-L1) and cervicothoracic (C3-C7) spinal cord. The solid component appeared hypointense in T1-weighted MRI sequences, hyperintense in the T2-weighted MRI sequences, and heterogeneous in MRI images enhanced with gadolinium contrast medium in both cases. Gross total resection was performed via a median laminectomy. Postoperative pathological examination confirmed the diagnosis of RGNT. In addition, extensive analysis of genetic mutations was performed to explore the relationship with glioma, including telomerase reverse transcriptase promoter, isocitrate dehydrogenase 1/2, BRAF-V600E, and O(6)-methylguanine-DNA methyltransferase promoter. No radiotherapy or chemotherapy were performed in these two cases. As of the latest follow-up, both patients had a good prognosis. Given the widely varying clinical characteristics of, prognosis of, and treatments for spinal tumors, differential diagnosis is of great importance before surgery. Consideration of the tumor location and the patient's age and sex, in combination with the imaging features, may be the best approach to narrowing the differential diagnosis. Surgery is the preferred treatment for RGNT. We do not recommend to implement adjuvant radiotherapy and chemotherapy in these patients except the invasive or recurrent tumors. Further examination and routine follow-up should be recommended to estimate the long-term prognosis.
[Mh] Termos MeSH primário: Neoplasias do Ventrículo Cerebral/secundário
Glioma/patologia
Neoplasias da Medula Espinal/patologia
Neoplasias da Medula Espinal/secundário
[Mh] Termos MeSH secundário: Adulto
Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo
Neoplasias do Ventrículo Cerebral/imunologia
Feminino
Proteína Glial Fibrilar Ácida/metabolismo
Glioma/diagnóstico por imagem
Glioma/imunologia
Seres Humanos
Isocitrato Desidrogenase/metabolismo
Antígeno Ki-67/metabolismo
Imagem por Ressonância Magnética
Proteínas Associadas aos Microtúbulos/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Fator de Transcrição 2 de Oligodendrócitos
Formação de Roseta
Medula Espinal/diagnóstico por imagem
Neoplasias da Medula Espinal/diagnóstico por imagem
Neoplasias da Medula Espinal/imunologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Glial Fibrillary Acidic Protein); 0 (Ki-67 Antigen); 0 (MAP2 protein, human); 0 (Microtubule-Associated Proteins); 0 (Nerve Tissue Proteins); 0 (OLIG2 protein, human); 0 (Oligodendrocyte Transcription Factor 2); EC 1.1.1.41 (Isocitrate Dehydrogenase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161205
[St] Status:MEDLINE


  10 / 477 MEDLINE  
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[PMID]:26517684
[Au] Autor:Tsigelny IF; Mukthavaram R; Kouznetsova VL; Chao Y; Babic I; Nurmemmedov E; Pastorino S; Jiang P; Calligaris D; Agar N; Scadeng M; Pingle SC; Wrasidlo W; Makale MT; Kesari S
[Ad] Endereço:Department of Neurosciences, University of California San Diego, La Jolla, CA, USA.
[Ti] Título:Multiple spatially related pharmacophores define small molecule inhibitors of OLIG2 in glioblastoma.
[So] Source:Oncotarget;8(14):22370-22384, 2017 Apr 04.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transcription factors (TFs) are a major class of protein signaling molecules that play key cellular roles in cancers such as the highly lethal brain cancer-glioblastoma (GBM). However, the development of specific TF inhibitors has proved difficult owing to expansive protein-protein interfaces and the absence of hydrophobic pockets. We uniquely defined the dimerization surface as an expansive parental pharmacophore comprised of several regional daughter pharmacophores. We targeted the OLIG2 TF which is essential for GBM survival and growth, we hypothesized that small molecules able to fit each subpharmacophore would inhibit OLIG2 activation. The most active compound was OLIG2 selective, it entered the brain, and it exhibited potent anti-GBM activity in cell-based assays and in pre-clinical mouse orthotopic models. These data suggest that (1) our multiple pharmacophore approach warrants further investigation, and (2) our most potent compounds merit detailed pharmacodynamic, biophysical, and mechanistic characterization for potential preclinical development as GBM therapeutics.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Fatores de Transcrição Hélice-Alça-Hélice Básicos/antagonistas & inibidores
Neoplasias Encefálicas/tratamento farmacológico
Desenho de Drogas
Glioblastoma/tratamento farmacológico
Guanidinas/uso terapêutico
Terapia de Alvo Molecular
Proteínas do Tecido Nervoso/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Fatores de Transcrição Hélice-Alça-Hélice Básicos/química
Processos de Crescimento Celular
Sobrevivência Celular/genética
Simulação por Computador
Seres Humanos
Camundongos
Camundongos Nus
Estrutura Molecular
Proteínas do Tecido Nervoso/química
Fator de Transcrição 2 de Oligodendrócitos
Ligação Proteica
Conformação Proteica
Bibliotecas de Moléculas Pequenas
Células Tumorais Cultivadas
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Guanidines); 0 (Nerve Tissue Proteins); 0 (OLIG2 protein, human); 0 (Oligodendrocyte Transcription Factor 2); 0 (Small Molecule Libraries); 21062-28-2 (1-(3,4-dichlorophenyl)-3-(4-((1-ethyl-3-piperidyl)amino)-6-methyl-2-pyrimidinyl)guanidine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151031
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.5633



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