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[PMID]:28456012
[Au] Autor:Alizadeh A; Dyck SM; Kataria H; Shahriary GM; Nguyen DH; Santhosh KT; Karimi-Abdolrezaee S
[Ad] Endereço:Regenerative Medicine Program, Department of Physiology and Pathophysiology, Spinal Cord Research Centre, University of Manitoba, Winnipeg, Manitoba, R3E 0J9, Canada.
[Ti] Título:Neuregulin-1 positively modulates glial response and improves neurological recovery following traumatic spinal cord injury.
[So] Source:Glia;65(7):1152-1175, 2017 Jul.
[Is] ISSN:1098-1136
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Spinal cord injury (SCI) results in glial activation and neuroinflammation, which play pivotal roles in the secondary injury mechanisms with both pro- and antiregeneration effects. Presently, little is known about the endogenous molecular mechanisms that regulate glial functions in the injured spinal cord. We previously reported that the expression of neuregulin-1 (Nrg-1) is acutely and chronically declined following traumatic SCI. Here, we investigated the potential ramifications of Nrg-1 dysregulation on glial and immune cell reactivity following SCI. Using complementary in vitro approaches and a clinically-relevant model of severe compressive SCI in rats, we demonstrate that immediate delivery of Nrg-1 (500 ng/day) after injury enhances a neuroprotective phenotype in inflammatory cells associated with increased interleukin-10 and arginase-1 expression. We also found a decrease in proinflammatory factors including IL-1ß, TNF-α, matrix metalloproteinases (MMP-2 and 9) and nitric oxide after injury. In addition, Nrg-1 modulates astrogliosis and scar formation by reducing inhibitory chondroitin sulfate proteoglycans after SCI. Mechanistically, Nrg-1 effects on activated glia are mediated through ErbB2 tyrosine phosphorylation in an ErbB2/3 heterodimer complex. Furthermore, Nrg-1 exerts its effects through downregulation of MyD88, a downstream adaptor of Toll-like receptors, and increased phosphorylation of Erk1/2 and STAT3. Nrg-1 treatment with the therapeutic dosage of 1.5 µg/day significantly improves tissue preservation and functional recovery following SCI. Our findings for the first time provide novel insights into the role and mechanisms of Nrg-1 in acute SCI and suggest a positive immunomodulatory role for Nrg-1 that can harness the beneficial properties of activated glia and inflammatory cells in recovery following SCI.
[Mh] Termos MeSH primário: Doenças do Sistema Nervoso/tratamento farmacológico
Doenças do Sistema Nervoso/etiologia
Neuregulina-1/uso terapêutico
Neuroglia/fisiologia
Recuperação de Função Fisiológica/fisiologia
Traumatismos da Medula Espinal/complicações
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Arginase/metabolismo
Células Cultivadas
Meios de Cultivo Condicionados/farmacologia
Modelos Animais de Doenças
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/fisiologia
Proteína Glial Fibrilar Ácida/metabolismo
Interleucina-10/metabolismo
Lipopolissacarídeos/toxicidade
Locomoção/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Neuregulina-1/metabolismo
Neuregulina-1/farmacologia
Neuroglia/efeitos dos fármacos
Ratos
Recuperação de Função Fisiológica/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Traumatismos da Medula Espinal/patologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Culture Media, Conditioned); 0 (Glial Fibrillary Acidic Protein); 0 (Lipopolysaccharides); 0 (Neuregulin-1); 130068-27-8 (Interleukin-10); EC 3.5.3.1 (Arginase); EC 3.5.3.1 (arginase I, rat)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.1002/glia.23150


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[PMID]:29339718
[Au] Autor:Parfejevs V; Debbache J; Shakhova O; Schaefer SM; Glausch M; Wegner M; Suter U; Riekstina U; Werner S; Sommer L
[Ad] Endereço:Institute of Anatomy, University of Zürich, 8057, Zürich, Switzerland.
[Ti] Título:Injury-activated glial cells promote wound healing of the adult skin in mice.
[So] Source:Nat Commun;9(1):236, 2018 01 16.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cutaneous wound healing is a complex process that aims to re-establish the original structure of the skin and its functions. Among other disorders, peripheral neuropathies are known to severely impair wound healing capabilities of the skin, revealing the importance of skin innervation for proper repair. Here, we report that peripheral glia are crucially involved in this process. Using a mouse model of wound healing, combined with in vivo fate mapping, we show that injury activates peripheral glia by promoting de-differentiation, cell-cycle re-entry and dissemination of the cells into the wound bed. Moreover, injury-activated glia upregulate the expression of many secreted factors previously associated with wound healing and promote myofibroblast differentiation by paracrine modulation of TGF-ß signalling. Accordingly, depletion of these cells impairs epithelial proliferation and wound closure through contraction, while their expansion promotes myofibroblast formation. Thus, injury-activated glia and/or their secretome might have therapeutic potential in human wound healing disorders.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Neuroglia/fisiologia
Pele/fisiopatologia
Cicatrização/fisiologia
[Mh] Termos MeSH secundário: Animais
Ciclo Celular/genética
Ciclo Celular/fisiologia
Diferenciação Celular/genética
Células Cultivadas
Perfilação da Expressão Gênica
Seres Humanos
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos DBA
Camundongos Knockout
Camundongos Transgênicos
Miofibroblastos/metabolismo
Miofibroblastos/fisiologia
Neuroglia/citologia
Neuroglia/metabolismo
Fatores de Transcrição SOXE/genética
Fatores de Transcrição SOXE/metabolismo
Transdução de Sinais/genética
Pele/lesões
Pele/inervação
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
Cicatrização/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (SOXE Transcription Factors); 0 (Sox10 protein, mouse); 0 (Transforming Growth Factor beta)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-01488-2


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[PMID]:29346405
[Au] Autor:Palanisamy A; Kannappan R; Xu Z; Martino A; Friese MB; Boyd JD; Crosby G; Culley DJ
[Ad] Endereço:Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.
[Ti] Título:Oxytocin alters cell fate selection of rat neural progenitor cells in vitro.
[So] Source:PLoS One;13(1):e0191160, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Synthetic oxytocin (sOT) is widely used during labor, yet little is known about its effects on fetal brain development despite evidence that it reaches the fetal circulation. Here, we tested the hypothesis that sOT would affect early neurodevelopment by investigating its effects on neural progenitor cells (NPC) from embryonic day 14 rat pups. NPCs expressed the oxytocin receptor (OXTR), which was downregulated by 45% upon prolonged treatment with sOT. Next, we examined the effects of sOT on NPC death, apoptosis, proliferation, and differentiation using antibodies to NeuN (neurons), Olig2 (oligodendrocytes), and GFAP (astrocytes). Treated NPCs were analysed with unbiased high-throughput immunocytochemistry. Neither 6 nor 24 h exposure to 100 pM or 100 nM sOT had an effect on viability as assessed by PI or CC-3 immunocytochemistry. Similarly, sOT had negligible effect on NPC proliferation, except that the overall rate of NPC proliferation was higher in the 24 h compared to the 6 h group regardless of sOT exposure. The most significant finding was that sOT exposure caused NPCs to select a predominantly neuronal lineage, along with a concomitant decrease in glial cells. Collectively, our data suggest that perinatal exposure to sOT can have neurodevelopmental consequences for the fetus, and support the need for in vivo anatomical and behavioral studies in offspring exposed to sOT in utero.
[Mh] Termos MeSH primário: Células-Tronco Neurais/efeitos dos fármacos
Ocitocina/toxicidade
[Mh] Termos MeSH secundário: Animais
Astrócitos/citologia
Astrócitos/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
Linhagem da Célula/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Regulação para Baixo/efeitos dos fármacos
Feminino
Seres Humanos
Células-Tronco Neurais/citologia
Células-Tronco Neurais/metabolismo
Neurogênese/efeitos dos fármacos
Neuroglia/citologia
Neuroglia/efeitos dos fármacos
Neurônios/citologia
Neurônios/efeitos dos fármacos
Oligodendroglia/citologia
Oligodendroglia/efeitos dos fármacos
Ocitocina/administração & dosagem
Ocitocina/metabolismo
Placenta/metabolismo
Gravidez
Efeitos Tardios da Exposição Pré-Natal
Ratos
Ratos Sprague-Dawley
Receptores de Ocitocina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, Oxytocin); 0 (oxytocin receptor, rat); 50-56-6 (Oxytocin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180119
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191160


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[PMID]:27772534
[Au] Autor:Keshavarz M
[Ad] Endereço:Shiraz Neuroscience Research Center,Shiraz University of Medical Sciences,Shiraz,Iran.
[Ti] Título:Glial cells as key elements in the pathophysiology and treatment of bipolar disorder.
[So] Source:Acta Neuropsychiatr;29(3):140-152, 2017 Jun.
[Is] ISSN:1601-5215
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The exact pathophysiology of bipolar disorder (BD) is not yet fully understood, and there are many questions in this area which should be answered. This review aims to discuss the roles of glial cells in the pathophysiology of BD and their contribution to the mechanism of action of mood-stabilising drugs. METHODS: We critically reviewed the most recent advances regarding glial cell roles in the pathophysiology and treatment of BD and the neuroprotective and neurotrophic effects of these cells. RESULTS: Postmortem studies revealed a decrease in the glial cell number or density in the specific layers of prefrontal and anterior cingulate cortex in the patients with BD, whereas there was no difference in other brain regions, such as entorhinal cortex, amygdala and hippocampus. Astrocytes and oligodendrocytes were the most important glial types that were responsible for the glial reduction, but microglia activation rather than loss may be implicated in BD. The decreased number or density of glial cells may contribute to the pathological changes observed in neurons in the patients with BD. Alteration of specific neurotrophic factors such as glial cell line-derived neurotrophic factor and S100B may be an important feature of BD. Glial cells mediate the therapeutic effects of mood-stabilising agents in the treatment of BD. CONCLUSION: Recent studies provide important evidence on the impairment of glial cells in the pathophysiology and treatment of BD. However, future controlled studies are necessary to elucidate different aspects of glial cells contribution to BD, and the mechanism of action of mood-stabilising drugs.
[Mh] Termos MeSH primário: Tonsila do Cerebelo/citologia
Transtorno Bipolar/fisiopatologia
Hipocampo/citologia
Neuroglia/fisiologia
[Mh] Termos MeSH secundário: Tonsila do Cerebelo/metabolismo
Tonsila do Cerebelo/patologia
Astrócitos/metabolismo
Astrócitos/patologia
Transtorno Bipolar/tratamento farmacológico
Encéfalo/patologia
Encéfalo/fisiopatologia
Diagnóstico
Fator Neurotrófico Derivado de Linhagem de Célula Glial/metabolismo
Hipocampo/metabolismo
Hipocampo/patologia
Seres Humanos
Transtornos do Humor/tratamento farmacológico
Neuroglia/citologia
Neuroglia/metabolismo
Neurônios/metabolismo
Neurônios/patologia
Oligodendroglia/metabolismo
Oligodendroglia/patologia
Subunidade beta da Proteína Ligante de Cálcio S100/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (GDNF protein, human); 0 (Glial Cell Line-Derived Neurotrophic Factor); 0 (S100 Calcium Binding Protein beta Subunit); 0 (S100B protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1017/neu.2016.56


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Barraviera, Benedito
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[PMID]:28450050
[Au] Autor:Araújo MR; Kyrylenko S; Spejo AB; Castro MV; Ferreira Junior RS; Barraviera B; Oliveira ALR
[Ad] Endereço:Department of Structural and Functional Biology, Institute of Biology, University of Campinas, Campinas, Sao Paulo, Brazil.
[Ti] Título:Transgenic human embryonic stem cells overexpressing FGF2 stimulate neuroprotection following spinal cord ventral root avulsion.
[So] Source:Exp Neurol;294:45-57, 2017 08.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ventral root avulsion (VRA) triggers a strong glial reaction which contributes to neuronal loss, as well as to synaptic detachment. To overcome the degenerative effects of VRA, treatments with neurotrophic factors and stem cells have been proposed. Thus, we investigated neuroprotection elicited by human embryonic stem cells (hESC), modified to overexpress a human fibroblast growth factor 2 (FGF-2), on motoneurons subjected to VRA. Lewis rats were submitted to VRA (L4-L6) and hESC/FGF-2 were applied to the injury site using a fibrin scaffold. The spinal cords were processed to evaluate neuronal survival, synaptic stability, and glial reactivity two weeks post lesion. Then, qRT-PCR was used to assess gene expression of ß2-microglobulin (ß2m), TNFα, IL1ß, IL6 and IL10 in the spinal cord in vivo and FGF2 mRNA levels in hESC in vitro. The results indicate that hESC overexpressing FGF2 significantly rescued avulsed motoneurons, preserving synaptic covering and reducing astroglial reactivity. The cells were also shown to express BDNF and GDNF at the site of injury. Additionally, engraftment of hESC led to a significant reduction in mRNA levels of TNFα at the spinal cord ventral horn, indicating their immunomodulatory properties. Overall, the present data suggest that hESC overexpressing FGF2 are neuroprotective and can shift gene expression towards an anti-inflammatory environment.
[Mh] Termos MeSH primário: Células-Tronco Embrionárias Humanas/transplante
Radiculopatia/cirurgia
Raízes Nervosas Espinhais/patologia
[Mh] Termos MeSH secundário: Animais
Movimento Celular
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/genética
Modelos Animais de Doenças
Doxiciclina/uso terapêutico
Feminino
Adesivo Tecidual de Fibrina/toxicidade
Fator 2 de Crescimento de Fibroblastos/genética
Fator 2 de Crescimento de Fibroblastos/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/genética
Vetores Genéticos/fisiologia
Células-Tronco Embrionárias Humanas/metabolismo
Seres Humanos
Neurônios Motores/metabolismo
Neurônios Motores/patologia
Proteínas do Tecido Nervoso/metabolismo
Neuroglia/efeitos dos fármacos
Neuroglia/metabolismo
Radiculopatia/induzido quimicamente
Ratos
Ratos Endogâmicos Lew
Adesivos Teciduais/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fibrin Tissue Adhesive); 0 (Nerve Tissue Proteins); 0 (Tissue Adhesives); 103107-01-3 (Fibroblast Growth Factor 2); N12000U13O (Doxycycline)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180218
[Lr] Data última revisão:
180218
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


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[PMID]:29322247
[Au] Autor:Han JW; Choi J; Kim YS; Kim J; Brinkmann R; Lyu J; Park TK
[Ad] Endereço:Department of Ophthalmology, College of Medicine, Soonchunhyang University, Bucheon, South Korea.
[Ti] Título:Comparison of the neuroinflammatory responses to selective retina therapy and continuous-wave laser photocoagulation in mouse eyes.
[So] Source:Graefes Arch Clin Exp Ophthalmol;256(2):341-353, 2018 Feb.
[Is] ISSN:1435-702X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: This study investigated microglia and inflammatory cell responses after selective retina therapy (SRT) with microsecond-pulsed laser in comparison to continuous-wave laser photocoagulation (cwPC). METHODS: Healthy C57BL/6 J mice were treated with either a train of short pulses (SRT; 527-nm, Q-switched, 1.7-µs pulse) or a conventional thermal continuous-wave (532-nm, 100-ms pulse duration) laser. The mice were sacrificed and their eyes were enucleated 1, 3, 7, and 14 days after both laser treatments. Pattern of cell death on retinal section was evaluated by TUNEL assay, and the distribution of activated inflammatory cells and glial cells were observed under immunohistochemistry. Consecutive changes for the expression of cytokines such as IL-1ß, TNF-α, and TGF-ß were also examined using immunohistochemistry, and compared among each period after quantification by Western blotting. RESULTS: The numbers of TUNEL-positive cells in the retinal pigment epithelium (RPE) layer did not differ in SRT and cwPC lesions, but TUNEL-positive cells in neural retinas were significantly less on SRT. Vague glial cell activation was observed in SRT-treated lesions. The population of inflammatory cells was also significantly decreased after SRT, and the cells were located in the RPE layer and subretinal space. Proinflammatory cytokines, including IL-1ß and TNF-α, showed significantly lower levels after SRT; conversely, the level of TGF-ß was similar to the cwPC-treated lesion. CONCLUSIONS: SRT resulted in selective RPE damage without collateral thermal injury to the neural retina, and apparently produced negligible glial activation. In addition, SRT showed a markedly less inflammatory response than cwPC, which may have important therapeutic implications for several macular diseases.
[Mh] Termos MeSH primário: Citocinas/biossíntese
Fotocoagulação a Laser/métodos
Lasers de Estado Sólido/uso terapêutico
Neuroglia/patologia
Doenças Retinianas/cirurgia
Epitélio Pigmentado da Retina/patologia
[Mh] Termos MeSH secundário: Animais
Apoptose
Western Blotting
Contagem de Células
Modelos Animais de Doenças
Angiofluoresceinografia/métodos
Fundo de Olho
Imuno-Histoquímica
Marcação In Situ das Extremidades Cortadas
Camundongos
Camundongos Endogâmicos C57BL
Neuroglia/metabolismo
Doenças Retinianas/diagnóstico
Doenças Retinianas/metabolismo
Epitélio Pigmentado da Retina/metabolismo
Tomografia de Coerência Óptica/métodos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1007/s00417-017-3883-7


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[PMID]:29291419
[Au] Autor:Liu Q; Qin Q; Sun H; Zhong D; An R; Tian Y; Chen H; Jin J; Wang H; Li G
[Ad] Endereço:Department of Neurology, The First Affiliated Hospital of Harbin Medical University, China.
[Ti] Título:Neuroprotective effect of olfactory ensheathing cells co-transfected with Nurr1 and Ngn2 in both in vitro and in vivo models of Parkinson's disease.
[So] Source:Life Sci;194:168-176, 2018 Feb 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: The aim of the study is to evaluate the neuroprotective effects of olfactory ensheathing cells (OECs) with the overexpression of nuclear receptor-related factor 1 (Nurr1) and neurogenin 2 (Ngn2) in experimental models of Parkinson's disease (PD) and to elucidate the potential mechanism underlying the neuroprotective effects of OECs-Nurr1-Ngn2. MATERIALS AND METHODS: In vitro study, OECs-Nurr1-Ngn2 conditioned medium (CM) was added to MPP -treated PC12 cells for 24h, and then the viability of PC12 cells, oxidative stress and apoptosis were detected. In vivo study, 48 male Sprague-Dawley (SD) rats were randomly divided into four groups. OECs/VMCs and OECs-Nurr1-Ngn2/VMCs groups were transplanted with 2×10 cells each of OECs or OECs-Nurr1-Ngn2 and VMCs into the right striatum one week after a unilateral 6-OHDA lesion. Control and PD groups were injected with 0.9% NaCl and 0.2% ascorbic acid into the same region. Rotational behavior was determined at 2, 4, 6 and 8weeks after injection or implantation in all groups. Neuronal differentiation markers, oxidative stress- and apoptosis-related indicators were detected at 8weeks post-grafting. KEY FINDINGS: OECs-Nurr1-Ngn2 increased the viability of PC12 cells, inhibited oxidative stress and apoptosis, and these effects could be reversed by pre-treatment of k252a, a TrkB receptor inhibitor. The behavioral deficits of PD rat were ameliorated by the transplantation of OECs-Nurr1-Ngn2/VMCs. SIGNIFICANCE: These results suggest that OECs-Nurr1-Ngn2 exhibits substantial neuroprotective, anti-oxidant, and anti-apoptotic effects against PD via the up-regulation of the neurotrophic factor-TrkB pathway.
[Mh] Termos MeSH primário: Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Proteínas do Tecido Nervoso/genética
Neuroglia/transplante
Membro 2 do Grupo A da Subfamília 4 de Receptores Nucleares/genética
Bulbo Olfatório/citologia
Doença de Parkinson/metabolismo
Doença de Parkinson/terapia
Transfecção
[Mh] Termos MeSH secundário: Animais
Fatores de Transcrição Hélice-Alça-Hélice Básicos/uso terapêutico
Células Cultivadas
Modelos Animais de Doenças
Terapia Genética/métodos
Masculino
Proteínas do Tecido Nervoso/uso terapêutico
Neuroglia/metabolismo
Neuroproteção
Membro 2 do Grupo A da Subfamília 4 de Receptores Nucleares/uso terapêutico
Células PC12
Doença de Parkinson/genética
Doença de Parkinson/patologia
Ratos
Ratos Sprague-Dawley
Transfecção/métodos
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Nerve Tissue Proteins); 0 (Ngn2 protein, rat); 0 (Nuclear Receptor Subfamily 4, Group A, Member 2)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180102
[St] Status:MEDLINE


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[PMID]:28457739
[Au] Autor:Oppliger B; Joerger-Messerli MS; Simillion C; Mueller M; Surbek DV; Schoeberlein A
[Ad] Endereço:Department of Obstetrics and Gynecology, Inselspital, Bern University Hospital, University of Bern, Switzerland; Department of Clinical Research, University of Bern, Switzerland.
[Ti] Título:Mesenchymal stromal cells from umbilical cord Wharton's jelly trigger oligodendroglial differentiation in neural progenitor cells through cell-to-cell contact.
[So] Source:Cytotherapy;19(7):829-838, 2017 07.
[Is] ISSN:1477-2566
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AIMS: Wharton's jelly mesenchymal stromal cells (WJ-MSCs) might be ideal candidates to treat perinatal brain damage. Their secretome has been shown to have beneficial effects on neuroregeneration, in part through interaction with neural progenitor cells (NPCs). However, it remains unclear whether cell-to-cell contact decisively contributes to this positive effect. The objective of this study was to elucidate the mechanism through which differentiation in NPCs is triggered after exposure to WJ-MSCs. Furthermore, given that WJ-MSCs can be derived from term (tWJ-MSCs) or preterm (ptWJ-MSCs) deliveries and that WJ-MSCs might be used for transplantations independent of gestational age, the influence of tWJ-MSCs versus ptWJ-MSCs on the differentiation capacities of NPCs was studied. METHODS: The effect of tWJ-MSCs and ptWJ-MSCs on the expression of neuroglial markers in NPCs was assessed in co-culture (CC), conditioned medium (CM) or transwell CC experiments by immunocytochemistry, real-time polymerase chain reaction and Western blot. Additionally, mass spectrometry was used to study their secretomes. RESULTS: NPCs showed an increased expression of glial markers after CC with WJ-MSCs or exposure to WJ-MSC-CMs. CC had a more prominent effect on the expression of glial markers compared with CM or transwell CCs. tWJ-MSCs more strongly induced the expression of mature oligodendroglial markers compared with ptWJ-MSCs. A possible role in enhancing this maturation could be attributed to the laminin α2-subunit. CONCLUSIONS: Cell-to-cell contact between WJ-MSCs and NPCs induces oligodendrogenesis on NPCs, whereas trophic factor secretion is sufficient to promote astrogenesis. Thus, transplanting WJ-MSCs may promote endogenous neuroregeneration in perinatal brain damage.
[Mh] Termos MeSH primário: Células Mesenquimais Estromais/citologia
Células-Tronco Neurais/citologia
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Comunicação Celular
Diferenciação Celular
Células Cultivadas
Meios de Cultivo Condicionados
Feminino
Seres Humanos
Células Mesenquimais Estromais/fisiologia
Células-Tronco Neurais/fisiologia
Neuroglia/citologia
Neuroglia/fisiologia
Oligodendroglia/citologia
Gravidez
Ratos
Cordão Umbilical/citologia
Geleia de Wharton/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Culture Media, Conditioned)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


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[PMID]:28470148
[Au] Autor:Kleinecke S; Richert S; de Hoz L; Brügger B; Kungl T; Asadollahi E; Quintes S; Blanz J; McGonigal R; Naseri K; Sereda MW; Sachsenheimer T; Lüchtenborg C; Möbius W; Willison H; Baes M; Nave KA; Kassmann CM
[Ad] Endereço:Department of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
[Ti] Título:Peroxisomal dysfunctions cause lysosomal storage and axonal Kv1 channel redistribution in peripheral neuropathy.
[So] Source:Elife;6, 2017 05 04.
[Is] ISSN:2050-084X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Impairment of peripheral nerve function is frequent in neurometabolic diseases, but mechanistically not well understood. Here, we report a novel disease mechanism and the finding that glial lipid metabolism is critical for axon function, independent of myelin itself. Surprisingly, nerves of Schwann cell-specific mutant mice were unaltered regarding axon numbers, axonal calibers, and myelin sheath thickness by electron microscopy. In search for a molecular mechanism, we revealed enhanced abundance and internodal expression of axonal membrane proteins normally restricted to juxtaparanodal lipid-rafts. Gangliosides were altered and enriched within an expanded lysosomal compartment of paranodal loops. We revealed the same pathological features in a mouse model of human Adrenomyeloneuropathy, preceding disease-onset by one year. Thus, peroxisomal dysfunction causes secondary failure of local lysosomes, thereby impairing the turnover of gangliosides in myelin. This reveals a new aspect of axon-glia interactions, with Schwann cell lipid metabolism regulating the anchorage of juxtaparanodal K 1-channels.
[Mh] Termos MeSH primário: Axônios/enzimologia
Metabolismo dos Lipídeos
Lisossomos/metabolismo
Neuroglia/metabolismo
Doenças do Sistema Nervoso Periférico/fisiopatologia
Peroxissomos/metabolismo
Canais de Potássio de Abertura Dependente da Tensão da Membrana/análise
[Mh] Termos MeSH secundário: Adrenoleucodistrofia/patologia
Animais
Axônios/ultraestrutura
Modelos Animais de Doenças
Seres Humanos
Camundongos
Microscopia Eletrônica
Receptor 1 de Sinal de Orientação para Peroxissomos/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Peroxisome-Targeting Signal 1 Receptor); 0 (Pex5 protein, mouse); 0 (Potassium Channels, Voltage-Gated)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180211
[Lr] Data última revisão:
180211
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


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[PMID]:29221753
[Au] Autor:Daniel DC; Johnson EM
[Ad] Endereço:Department of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, VA 23507, USA.
[Ti] Título:PURA, the gene encoding Pur-alpha, member of an ancient nucleic acid-binding protein family with mammalian neurological functions.
[So] Source:Gene;643:133-143, 2018 Feb 15.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The PURA gene encodes Pur-alpha, a 322 amino acid protein with repeated nucleic acid binding domains that are highly conserved from bacteria through humans. PUR genes with a single copy of this domain have been detected so far in spirochetes and bacteroides. Lower eukaryotes possess one copy of the PUR gene, whereas chordates possess 1 to 4 PUR family members. Human PUR genes encode Pur-alpha (Pura), Pur-beta (Purb) and two forms of Pur-gamma (Purg). Pur-alpha is a protein that binds specific DNA and RNA sequence elements. Human PURA, located at chromosome band 5q31, is under complex control of three promoters. The entire protein coding sequence of PURA is contiguous within a single exon. Several studies have found that overexpression or microinjection of Pura inhibits anchorage-independent growth of oncogenically transformed cells and blocks proliferation at either G1-S or G2-M checkpoints. Effects on the cell cycle may be mediated by interaction of Pura with cellular proteins including Cyclin/Cdk complexes and the Rb tumor suppressor protein. PURA knockout mice die shortly after birth with effects on brain and hematopoietic development. In humans environmentally induced heterozygous deletions of PURA have been implicated in forms of myelodysplastic syndrome and progression to acute myelogenous leukemia. Pura plays a role in AIDS through association with the HIV-1 protein, Tat. In the brain Tat and Pura association in glial cells activates transcription and replication of JC polyomavirus, the agent causing the demyelination disease, progressive multifocal leukoencephalopathy. Tat and Pura also act to stimulate replication of the HIV-1 RNA genome. In neurons Pura accompanies mRNA transcripts to sites of translation in dendrites. Microdeletions in the PURA locus have been implicated in several neurological disorders. De novo PURA mutations have been related to a spectrum of phenotypes indicating a potential PURA syndrome. The nucleic acid, G-rich Pura binding element is amplified as expanded polynucleotide repeats in several brain diseases including fragile X syndrome and a familial form of amyotrophic lateral sclerosis/fronto-temporal dementia. Throughout evolution the Pura protein plays a critical role in survival, based on conservation of its nucleic acid binding properties. These Pura properties have been adapted in higher organisms to the as yet unfathomable development of the human brain.
[Mh] Termos MeSH primário: Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos/genética
Animais
Sequência de Bases
Ciclo Celular
Proteínas de Ciclo Celular/genética
Sequência Conservada/genética
Replicação do DNA
Células Dendríticas/metabolismo
HIV-1/genética
Seres Humanos
Leucemia Mieloide Aguda/genética
Síndromes Mielodisplásicas/genética
Neuroglia/metabolismo
Neurônios/metabolismo
Proteínas com Motivo de Reconhecimento de RNA/genética
Proteínas com Motivo de Reconhecimento de RNA/metabolismo
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (DNA-Binding Proteins); 0 (PURA protein, human); 0 (RNA Recognition Motif Proteins); 0 (RNA, Messenger); 0 (Transcription Factors)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180210
[Lr] Data última revisão:
180210
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171210
[St] Status:MEDLINE



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