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Pesquisa : D12.776.543.620.738 [Categoria DeCS]
Referências encontradas : 684 [refinar]
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[PMID]:28943240
[Au] Autor:Kempf A; Boda E; Kwok JCF; Fritz R; Grande V; Kaelin AM; Ristic Z; Schmandke A; Schmandke A; Tews B; Fawcett JW; Pertz O; Buffo A; Schwab ME
[Ad] Endereço:Brain Research Institute, University of Zurich and Department of Health Sciences and Technology, Swiss Federal Institute of Technology (ETH) Zurich, 8057 Zurich, Switzerland. Electronic address: anissa.kempf@cncb.ox.ac.uk.
[Ti] Título:Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction.
[So] Source:Dev Cell;43(1):24-34.e5, 2017 Oct 09.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes. Here, we show that the transmembrane protein, Nogo-A, inhibits neurite outgrowth and cell spreading in neurons and Nogo-A-responsive cell lines via HSPGs. The extracellular, active 180 amino acid Nogo-A region, named Nogo-A-Δ20, binds to heparin and brain-derived heparan sulfate glycosaminoglycans (GAGs) but not to the closely related chondroitin sulfate GAGs. HSPGs are required for Nogo-A-Δ20-induced inhibition of adhesion, cell spreading, and neurite outgrowth, as well as for RhoA activation. Surprisingly, we show that Nogo-A-Δ20 can act via HSPGs independently of its receptor, Sphingosine-1-Phosphate receptor 2 (S1PR2). We thereby identify the HSPG family members syndecan-3 and syndecan-4 as functional receptors for Nogo-A-Δ20. Finally, we show in explant cultures ex vivo that Nogo-A-Δ20 promotes the migration of neuroblasts via HSPGs but not S1PR2.
[Mh] Termos MeSH primário: Movimento Celular/fisiologia
Forma Celular/fisiologia
Proteoglicanas de Heparan Sulfato/metabolismo
Neuritos/metabolismo
Crescimento Neuronal/fisiologia
Proteínas Nogo/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteínas de Transporte/metabolismo
Linhagem Celular
Células Cultivadas
Heparitina Sulfato/metabolismo
Camundongos
Ligação Proteica
Proteoglicanas/metabolismo
Receptores de Lisoesfingolipídeo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (Heparan Sulfate Proteoglycans); 0 (Nogo Proteins); 0 (Proteoglycans); 0 (Receptors, Lysosphingolipid); 9050-30-0 (Heparitin Sulfate)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE


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[PMID]:28880879
[Au] Autor:Takase H; Kurihara Y; Yokoyama TA; Kawahara N; Takei K
[Ad] Endereço:Department of Neurosurgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
[Ti] Título:LOTUS overexpression accelerates neuronal plasticity after focal brain ischemia in mice.
[So] Source:PLoS One;12(9):e0184258, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nogo receptor-1 (NgR1) and its ligands inhibit neuronal plasticity and limit functional recovery after brain damage such as ischemic stroke. We have previously shown that lateral olfactory tract usher substance (LOTUS) antagonizes NgR1-mediated signaling. Here, we investigated whether LOTUS enhances neuronal plasticity and functional recovery after brain focal ischemia in adult mice. Focal ischemic infarcts were induced in wild-type and LOTUS-overexpressing transgenic mice via middle cerebral artery occlusion. Endogenous LOTUS expression was increased in brain and cervical spinal cord of the contralateral side of ischemia in the chronic phase after brain ischemia. LOTUS overexpression accelerated midline-crossing axonal sprouting from the contralateral side to the ipsilateral side of ischemia in the medullar reticular formation and gray matter of denervated cervical spinal cord. Importantly, LOTUS overexpression improved neurological score highly correlated with laterality ratio of corticoreticular fibers of the medulla oblongata, indicating that LOTUS overexpression may overcome the inhibitory environment induced by NgR1 signaling for damaged motor pathway reconstruction after ischemic stroke. Thus, our data suggest that LOTUS overexpression accelerates neuronal plasticity in the brainstem and cervical spinal cord after stroke and LOTUS administration is useful for future therapeutic strategies.
[Mh] Termos MeSH primário: Isquemia Encefálica/metabolismo
Proteínas de Ligação ao Cálcio/metabolismo
Plasticidade Neuronal/fisiologia
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Encéfalo/patologia
Lesões Encefálicas/metabolismo
Lesões Encefálicas/patologia
Isquemia Encefálica/genética
Proteínas de Ligação ao Cálcio/genética
Medula Cervical/metabolismo
Modelos Animais de Doenças
Immunoblotting
Infarto da Artéria Cerebral Média/genética
Infarto da Artéria Cerebral Média/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Plasticidade Neuronal/genética
Proteínas Nogo/genética
Proteínas Nogo/metabolismo
Receptor Nogo 1/genética
Receptor Nogo 1/metabolismo
Acidente Vascular Cerebral/genética
Acidente Vascular Cerebral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium-Binding Proteins); 0 (Crtac1 protein, mouse); 0 (Nogo Proteins); 0 (Nogo Receptor 1); 0 (Rtn4r protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170908
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184258


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[PMID]:28807492
[Au] Autor:Lei HW; Wang JY; Dang QJ; Yang F; Liu X; Zhang JH; Li Y
[Ad] Endereço:Department of Rheumatology and Immunology, The Second Affiliated Hospital of Harbin Medical University, Harbin 150001, PR China.
[Ti] Título:Neuropsychiatric involvement in lupus is associated with the Nogo-a/NgR1 pathway.
[So] Source:J Neuroimmunol;311:22-28, 2017 Oct 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Neuroinflammation- and neurodegeneration-induced nerve injury may represent important components of neuropsychiatric lupus (NPSLE). Myelin-associated neurite outgrowth inhibitor (Nogo)-a and its receptor, NgR1, limit recovery of the adult central nervous system after injury. We detected a soluble Nogo-a product in the cerebral spinal fluid of patients with NPSLE. In a mouse model of lupus, aging was associated with an increase in Nogo-a positive neurons, diminished myelin sheaths, enhanced pro-inflammatory cytokines, and impaired cognition and memory. Treatment with the Nogo-66 antagonist promoted myelin repair, improved cognition and memory, and downregulated pro-inflammatory factors. Our data imply the Nogo-a/NgR1 pathway is involved in NPSLE.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Vasculite Associada ao Lúpus do Sistema Nervoso Central/metabolismo
Vasculite Associada ao Lúpus do Sistema Nervoso Central/patologia
Proteínas Nogo/metabolismo
Receptor Nogo 1/metabolismo
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Adulto
Animais
Encéfalo/patologia
Citocinas/genética
Citocinas/metabolismo
Modelos Animais de Doenças
Feminino
Seres Humanos
Vasculite Associada ao Lúpus do Sistema Nervoso Central/tratamento farmacológico
Vasculite Associada ao Lúpus do Sistema Nervoso Central/genética
Masculino
Aprendizagem em Labirinto/fisiologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Meia-Idade
Proteínas da Mielina/uso terapêutico
Neurônios/metabolismo
Proteínas Nogo/genética
Receptor Nogo 1/genética
Fragmentos de Peptídeos/uso terapêutico
Estudos Retrospectivos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Myelin Proteins); 0 (NEP1-40 protein, human); 0 (Nogo Proteins); 0 (Nogo Receptor 1); 0 (Peptide Fragments)
[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:170816
[St] Status:MEDLINE


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[PMID]:28789474
[Au] Autor:Shepherd DJ; Tsai SY; Cappucci SP; Wu JY; Farrer RG; Kartje GL
[Ad] Endereço:Loyola University Health Sciences Division, Maywood, Illinois (DJS, SPC, GLK); and Edward Hines Jr. Veterans Affairs Hospital, Research Service, Hines, Illinois (DJS, S-YT, SPC, JYW, RGF, GLK).
[Ti] Título:The Subventricular Zone Response to Stroke Is Not a Therapeutic Target of Anti-Nogo-A Immunotherapy.
[So] Source:J Neuropathol Exp Neurol;76(8):683-696, 2017 Aug 01.
[Is] ISSN:1554-6578
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Ischemic stroke is a leading cause of adult disability with no pharmacological treatments to promote the recovery of lost function. Neutralizing antibodies against the neurite outgrowth inhibitor Nogo-A have emerged as a promising treatment for subacute and chronic stroke in animal models; however, whether anti-Nogo-A treatment affects poststroke neurogenesis remains poorly understood. In this study, we confirmed expression of Nogo-A by neuroblasts in the adult rat subventricular zone (SVZ), a major neurogenic niche; however, we found no evidence that Nogo-A was expressed at the surface of these cells. In vitro migration assays demonstrated that Nogo-A signaling induced a modest reduction in neuroblast migration speed, while anti-Nogo-A antibodies had no effect on motility properties. Using a permanent distal middle cerebral artery occlusion model of cortical stroke, we found that the number of proliferating cells in the SVZ was unaffected in response to stroke, while neuroblast mobilization from the SVZ toward the stroke lesion correlated positively with lesion size. However, we found no evidence that proliferation or neuroblast mobilization were affected by anti-Nogo-A antibody treatment. Our results suggest that the SVZ is not a therapeutic target of anti-Nogo-A immunotherapy, and contribute to our understanding of the SVZ response to cortical stroke.
[Mh] Termos MeSH primário: Anticorpos/farmacologia
Anticorpos/uso terapêutico
Infarto da Artéria Cerebral Média/tratamento farmacológico
Ventrículos Laterais/efeitos dos fármacos
Proteínas Nogo/imunologia
[Mh] Termos MeSH secundário: Animais
Bromodesoxiuridina/metabolismo
Movimento Celular/efeitos dos fármacos
Ciclosporina/imunologia
Modelos Animais de Doenças
Lateralidade Funcional
Técnicas In Vitro
Infusões Intraventriculares
Ventrículos Laterais/citologia
Masculino
Proteínas do Tecido Nervoso/metabolismo
Proteínas Nogo/metabolismo
Receptor Nogo 1/metabolismo
Técnicas de Cultura de Órgãos
Ratos
Ratos Long-Evans
Receptores de Lisoesfingolipídeo/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Nerve Tissue Proteins); 0 (Nogo Proteins); 0 (Nogo Receptor 1); 0 (Receptors, Lysosphingolipid); 0 (Rtn4r protein, rat); 0 (sphingosine-1-phosphate receptor-2, rat); 83HN0GTJ6D (Cyclosporine); G34N38R2N1 (Bromodeoxyuridine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.1093/jnen/nlx050


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[PMID]:28668079
[Au] Autor:Fang L; Wang Y; Zheng Q; Yang T; Zhao P; Zhao H; Zhang Q; Zhao Y; Qi F; Li K; Chen Z; Li J; Zhang N; Fan Y; Wang L
[Ad] Endereço:School of Traditional Chinese Medicine, Beijing Key Lab of TCM Collateral Disease Theory Research, Capital Medical University, Beijing, 100069, People's Republic of China.
[Ti] Título:Effects of Bu Shen Yi sui capsule on NogoA/NgR and its signaling pathways RhoA/ROCK in mice with experimental autoimmune encephalomyelitis.
[So] Source:BMC Complement Altern Med;17(1):346, 2017 Jul 01.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Axon growth inhibitory factors NogoA/Nogo receptor (NgR) and its signaling pathways RhoA/Rho kinase (ROCK) play a critical role in the repair of nerve damage in multiple sclerosis (MS). Bu Shen Yi Sui Capsule (BSYSC) is an effective Chinese formula utilized to treat MS in clinical setting and noted for its potent neuroprotective effects. In this study, we focus on the effects of BSYSC on promoting nerve repair and the underlying mechanisms in mice with experimental autoimmune encephalomyelitis (EAE), an animal model of MS. METHODS: The EAE mouse model was induced by injecting subcutaneously with myelin oligodendrocyte glycoprotein (MOG) supplemented with pertussis toxin. BSYSC was orally administrated at dose of 3.0 g/kg once a day for 40 days. The levels of protein gene product (PGP) 9.5, p-Tau, growth associated protein (GAP) -43, KI67 and Nestin in the brain or spinal cord on 20 and 40 day post-induction (dpi) were detected via immunofluorescence and Western blot analysis. Furthermore, NogoA/NgR and RhoA/ROCK signaling molecules were studied by qRT-PCR and Western blot analysis. RESULTS: Twenty or 40 days of treatment with BSYSC increased markedly PGP9.5 and GAP-43 levels, reduced p-Tau in the brain or spinal cord of mice with EAE. In addition, BSYSC elevated significantly the expression of KI67 and Nestin in the spinal cord 40 dpi. Further study showed that the activation of NogoA/NgR and RhoA/ROCK were suppressed by the presence of BSYSC. CONCLUSIONS: BSYSC could attenuate axonal injury and promote repair of axonal damage in EAE mice in part through the down-regulation of NogoA/NgR and RhoA/ROCK signaling pathways.
[Mh] Termos MeSH primário: Medicamentos de Ervas Chinesas/administração & dosagem
Encefalomielite Autoimune Experimental/tratamento farmacológico
Proteínas Nogo/metabolismo
Receptores Nogo/metabolismo
Quinases Associadas a rho/metabolismo
Proteína rhoA de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Animais
Encefalomielite Autoimune Experimental/genética
Encefalomielite Autoimune Experimental/metabolismo
Feminino
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Proteínas Nogo/genética
Receptores Nogo/genética
Transdução de Sinais
Quinases Associadas a rho/genética
Proteína rhoA de Ligação ao GTP/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drugs, Chinese Herbal); 0 (Nogo Proteins); 0 (Nogo Receptors); EC 2.7.11.1 (rho-Associated Kinases); EC 3.6.5.2 (rhoA GTP-Binding Protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170703
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-1847-4


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[PMID]:28640888
[Au] Autor:Alhusban A; Kozak A; Pillai B; Ahmed H; Sayed MA; Johnson MH; Ishrat T; Ergul A; Fagan SC
[Ad] Endereço:Program in Clinical and Experimental Therapeutics- Charlie Norwood VA Medical Center and College of Pharmacy, University of Georgia, Augusta, Georgia, United States of America.
[Ti] Título:Mechanisms of acute neurovascular protection with AT1 blockade after stroke: Effect of prestroke hypertension.
[So] Source:PLoS One;12(6):e0178867, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Stroke is a leading cause of adult disability worldwide. Improving stroke outcome requires an orchestrated interplay that involves up regulation of pro-survival pathways and a concomitant suppression of pro-apoptotic mediators. In this investigation, we assessed the involvement of eNOS in the AT1 blocker-mediated protective and pro-recovery effects in animals with hypertension. We also evaluated the effect of acute eNOS inhibition in hypertensive animals. To achieve these goals, spontaneously hypertensive rats (SHR) were implanted with blood pressure transmitters, and randomized to receive either an eNOS inhibitor (L-NIO) or saline one hour before cerebral ischemia induction. After 3 hours of ischemia, animals were further randomized to receive either candesartan or saline at the time of reperfusion and sacrificed either 24 hours or 7 days later. Candesartan induced an early protective effect that was independent of eNOS inhibition (50% improvement in motor function). However, the protective effect of candesartan was associated with about five fold up regulation of BDNF expression and about three fold reduction in ER stress markers, in an eNOS dependent manner. The early benefit of a single dose of candesartan, present at 24 hours after stroke, was diminished at 7 days, perhaps due to a failure to induce an angiogenic response in these hypertensive animals. In conclusion, our findings demonstrate an early prorecovery effect of candesartan at both functional and molecular levels. Candesartan induced prorecovery signaling was mediated through eNOS. This effect was not maintained at 7 days after experimental ischemia.
[Mh] Termos MeSH primário: Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Benzimidazóis/farmacologia
Vasos Sanguíneos/efeitos dos fármacos
Hipertensão/complicações
Fármacos Neuroprotetores/farmacologia
Receptor Tipo 1 de Angiotensina/metabolismo
Acidente Vascular Cerebral/prevenção & controle
Tetrazóis/farmacologia
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Vasos Sanguíneos/metabolismo
Vasos Sanguíneos/patologia
Vasos Sanguíneos/fisiopatologia
Fator Neurotrófico Derivado do Encéfalo/metabolismo
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Regulação da Expressão Gênica/efeitos dos fármacos
Masculino
Fatores de Crescimento Neural/metabolismo
Óxido Nítrico Sintase Tipo I/metabolismo
Óxido Nítrico Sintase Tipo III/antagonistas & inibidores
Óxido Nítrico Sintase Tipo III/metabolismo
Proteínas Nogo/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Proteínas Tirosina Quinases/metabolismo
Ratos
Ratos Endogâmicos SHR
Espécies Reativas de Nitrogênio/metabolismo
Receptor trkB
Transdução de Sinais/efeitos dos fármacos
Acidente Vascular Cerebral/metabolismo
Acidente Vascular Cerebral/patologia
Acidente Vascular Cerebral/fisiopatologia
Resposta a Proteínas não Dobradas/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Benzimidazoles); 0 (Brain-Derived Neurotrophic Factor); 0 (Nerve Growth Factors); 0 (Neuroprotective Agents); 0 (Nogo Proteins); 0 (Reactive Nitrogen Species); 0 (Receptor, Angiotensin, Type 1); 0 (Tetrazoles); EC 1.14.13.39 (Nitric Oxide Synthase Type I); EC 1.14.13.39 (Nitric Oxide Synthase Type III); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.1 (Receptor, trkB); EC 2.7.10.1 (TrkB protein, rat); S8Q36MD2XX (candesartan)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171122
[Lr] Data última revisão:
171122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178867


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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]:28341461
[Au] Autor:Chen K; Marsh BC; Cowan M; Al'Joboori YD; Gigout S; Smith CC; Messenger N; Gamper N; Schwab ME; Ichiyama RM
[Ad] Endereço:School of Biomedical Sciences, University of Leeds, Leeds LS2 9JT, United Kingdom; School of Biological Science and Medical Engineering, Beihang University, Beijing 100191, China.
[Ti] Título:Sequential therapy of anti-Nogo-A antibody treatment and treadmill training leads to cumulative improvements after spinal cord injury in rats.
[So] Source:Exp Neurol;292:135-144, 2017 Jun.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Intense training is the most clinically successful treatment modality following incomplete spinal cord injuries (SCIs). With the advent of plasticity enhancing treatments, understanding how treatments might interact when delivered in combination becomes critical. Here, we investigated a rational approach to sequentially combine treadmill locomotor training with antibody mediated suppression of the fiber growth inhibitory protein Nogo-A. Following a large but incomplete thoracic lesion, rats were immediately treated with either anti-Nogo-A or control antibody (2weeks) and then either left untrained or step-trained starting 3weeks after injury for 8weeks. It was found that sequentially combined therapy improved step consistency and reduced toe dragging and climbing errors, as seen with training and anti-Nogo-A individually. Animals with sequential therapy also adopted a more parallel paw position during bipedal walking and showed greater overall quadrupedal locomotor recovery than individual treatments. Histologically, sequential therapy induced the greatest corticospinal tract sprouting caudally into the lumbar region and increased the number of serotonergic synapses onto lumbar motoneurons. Increased primary afferent sprouting and synapse formation onto lumbar motoneurons observed with anti-Nogo-A antibody were reduced by training. Animals with sequential therapy also showed the highest reduction of lumbar interneuronal activity associated with walking (c-fos expression). No treatment effects for thermal nociception, mechanical allodynia, or lesion volume were observed. The results demonstrate that sequential administration of anti-Nogo-A antibody followed in time with intensive locomotor training leads to superior recovery of lost locomotor functions, which is probably mediated by changes in the interaction between descending sprouting and local segmental networks after SCI.
[Mh] Termos MeSH primário: Anticorpos/farmacologia
Locomoção/efeitos dos fármacos
Regeneração Nervosa/efeitos dos fármacos
Tratos Piramidais/efeitos dos fármacos
Recuperação de Função Fisiológica/efeitos dos fármacos
Traumatismos da Medula Espinal/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Feminino
Atividade Motora/efeitos dos fármacos
Atividade Motora/fisiologia
Proteínas da Mielina/metabolismo
Plasticidade Neuronal/efeitos dos fármacos
Plasticidade Neuronal/fisiologia
Proteínas Nogo/imunologia
Proteínas Nogo/metabolismo
Condicionamento Físico Animal
Ratos Sprague-Dawley
Recuperação de Função Fisiológica/fisiologia
Traumatismos da Medula Espinal/patologia
Traumatismos da Medula Espinal/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Myelin Proteins); 0 (Nogo Proteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170728
[Lr] Data última revisão:
170728
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170326
[St] Status:MEDLINE


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[PMID]:28228044
[Au] Autor:Yan X; Huang G; Liu Q; Zheng J; Chen H; Huang Q; Chen J; Huang H
[Ad] Endereço:a Department of Neurosurgery , the Fourth Affiliated Hospital of Guangxi Medical University , Liuzhou , China.
[Ti] Título:Withaferin A protects against spinal cord injury by inhibiting apoptosis and inflammation in mice.
[So] Source:Pharm Biol;55(1):1171-1176, 2017 Dec.
[Is] ISSN:1744-5116
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:CONTEXT: Withaferin A (WFA) exhibits diverse pharmaceutical applications on human diseases, including rheumatoid arthritis, cancers and microbial infection. OBJECTIVE: We evaluated the neuroprotective role of WFA using a mouse model of spinal cord injury (SCI). MATERIALS AND METHODS: BALB/c mice were administrated 10 mg/kg of WFA. Gene expression was measured by real-time PCR, western blot and immunohistochemistry. Cell morphology and apoptosis were determined by H&E staining and TUNEL assay. Motor function was evaluated by the BBB functional scale for continuous 7 weeks. RESULTS: WFA significantly improved neurobehavioural function and alleviated histological alteration of spinal cord tissues in traumatized mice. Brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) significantly increased in WFA-treated mice. Meanwhile, the expression of Nogo-A and RhoA remarkably decreased in the presence of WFA. Furthermore, the apoptotic cell death was attenuated in mice treated with WFA (31.48 ± 2.50% vs. 50.08 ± 2.08%) accompanied by decreased bax and increased bcl-2. In addition, WFA decreased the expression of pro-inflammatory mediators such as IL-1ß (11.20 ± 1.96 ng/mL vs. 17.59 ± 1.42 ng/mL) and TNF-α (57.38 ± 3.57 pg/mL vs. 95.06 ± 9.13 pg/mL). The anti-inflammatory cytokines including TGF-ß1 (14.32 ± 1.04 pg/mL vs. 9.37 ± 1.17 pg/mL) and IL-10 (116.80 ± 6.91 pg/mL vs. 72.33 ± 9.35 pg/mL) were elevated after WFA administration. DISCUSSION AND CONCLUSION: This study demonstrated that WFA has a neuroprotective role by inhibition of apoptosis and inflammation after SCI in mice.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Apoptose/efeitos dos fármacos
Inflamação/prevenção & controle
Fármacos Neuroprotetores/farmacologia
Traumatismos da Medula Espinal/tratamento farmacológico
Medula Espinal/efeitos dos fármacos
Vitanolídeos/farmacologia
[Mh] Termos MeSH secundário: Animais
Proteínas Reguladoras de Apoptose/metabolismo
Comportamento Animal/efeitos dos fármacos
Fator Neurotrófico Derivado do Encéfalo/metabolismo
Modelos Animais de Doenças
Fator Neurotrófico Derivado de Linhagem de Célula Glial/metabolismo
Inflamação/metabolismo
Inflamação/patologia
Inflamação/fisiopatologia
Mediadores da Inflamação/metabolismo
Camundongos Endogâmicos BALB C
Atividade Motora/efeitos dos fármacos
Proteínas Nogo/metabolismo
Transdução de Sinais/efeitos dos fármacos
Medula Espinal/metabolismo
Medula Espinal/patologia
Medula Espinal/fisiopatologia
Traumatismos da Medula Espinal/metabolismo
Traumatismos da Medula Espinal/patologia
Traumatismos da Medula Espinal/fisiopatologia
Fatores de Tempo
Proteínas rho de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Apoptosis Regulatory Proteins); 0 (Brain-Derived Neurotrophic Factor); 0 (Glial Cell Line-Derived Neurotrophic Factor); 0 (Inflammation Mediators); 0 (Neuroprotective Agents); 0 (Nogo Proteins); 0 (Rtn4 protein, mouse); 0 (Withanolides); EC 3.6.5.2 (RhoA protein, mouse); EC 3.6.5.2 (rho GTP-Binding Proteins); L6DO3QW4K5 (withaferin A)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170309
[Lr] Data última revisão:
170309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170224
[St] Status:MEDLINE
[do] DOI:10.1080/13880209.2017.1288262


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[PMID]:28214833
[Au] Autor:Zhu Y; Tong Q; Ye J; Ning Y; Xiong Y; Yang M; Xiao H; Lu J; Xu W; Li J; Li Q
[Ti] Título:Nogo-B Facilitates LPS-Mediated Immune Responses by Up-Regulation of TLR4-Signaling in Macrophage RAW264.7.
[So] Source:Cell Physiol Biochem;41(1):274-285, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Nogo-B, a member of the reticulon family of proteins, is mainly located in the endoplasmic reticulum (ER). Here, we investigate the function and mechanism of Nogo-B in the regulation of TLR4-associated immune responses in the macrophage cell line of RAW264.7. METHODS: Nogo-B was up- and down-regulated through the use of appropriate adenoviral vectors or siRNA, and the effects of Nogo-B on macrophages under liposaccharide (LPS) stimulation were evaluated via western blotting, immunofluorescence, enzyme-linked immunosorbent assay (ELISA), flow cytometric analysis, and transwell assay. RESULTS: Our data indicates that the protein of Nogo-B was down-regulated in a time- and dose-dependent manner following LPS administration in the macrophage. Nogo-B overexpression increased the production of inflammatory cytokines (MCP-1, TNF-α, IL-1ß, and TGF-ß), enhanced macrophage migration activities, activated major histocompatibility complex II (MHC II), and elevated the expression of macrophage scavenger receptor 1(MSR1), all of which suggest that Nogo-B is necessary for immune responses and plays an important role in regulating macrophage recruitment. Mechanistically, Nogo-B may enhance TLR4 expression in macrophage surfaces, activate mitogen-activated protein kinase (MAPK) pathways, and initiate inflammatory responses. CONCLUSION: These findings illustrate the key regulatory functions of Nogo-B in facilitating LPS-mediated immune responses through promoting the phosphorylation of MAP kinase.
[Mh] Termos MeSH primário: Lipopolissacarídeos/toxicidade
Proteínas Nogo/metabolismo
Transdução de Sinais/efeitos dos fármacos
Regulação para Cima/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Movimento Celular/efeitos dos fármacos
Citocinas/análise
Citocinas/genética
Citocinas/metabolismo
Ensaio de Imunoadsorção Enzimática
Macrófagos/citologia
Macrófagos/efeitos dos fármacos
Macrófagos/metabolismo
Camundongos
Microscopia de Fluorescência
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Proteínas Nogo/antagonistas & inibidores
Proteínas Nogo/genética
Células RAW 264.7
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Receptores Depuradores Classe A/metabolismo
Receptor 4 Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Lipopolysaccharides); 0 (Msr1 protein, mouse); 0 (Nogo Proteins); 0 (RNA, Small Interfering); 0 (Scavenger Receptors, Class A); 0 (Toll-Like Receptor 4); EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170606
[Lr] Data última revisão:
170606
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170220
[St] Status:MEDLINE
[do] DOI:10.1159/000456094



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