Base de dados : MEDLINE
Pesquisa : A11.872.653 [Categoria DeCS]
Referências encontradas : 7231 [refinar]
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[PMID]:29353044
[Au] Autor:Yamamoto H; Kurachi M; Naruse M; Shibasaki K; Ishizaki Y
[Ad] Endereço:Department of Molecular and Cellular Neurobiology, Gunma University Graduate School of Medicine, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan.
[Ti] Título:BMP4 signaling in NPCs upregulates Bcl-xL to promote their survival in the presence of FGF-2.
[So] Source:Biochem Biophys Res Commun;496(2):588-593, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We previously reported that BMP4 does not promote proliferation or differentiation of CD44-positive astrocyte precursor cells (APCs) but greatly promotes their survival in the presence of fibroblast growth factor-2 (FGF-2). In this study, we examined if BMP4 acts as a survival factor also for neural stem/progenitor cells (NPCs) isolated from ganglionic eminence of neonatal mouse brain. We found BMP4 promotes survival but not proliferation or differentiation of these cells, just as in the case for CD44-positive APCs. Microarray analysis revealed some candidate molecules in the signaling pathway downstream of BMP4. Among them, we focused on Id1 (inhibitor of DNA-binding 1) and Bcl-xL in this study. Expression of both genes was promoted in the presence of BMP4, and this promotion was reduced by dorsomorphin, an inhibitor of BMP4 signaling. Furthermore, cytochrome c release from mitochondria was significantly reduced in the presence of BMP4, suggesting up-regulation of Bcl-xL activity by BMP4. Id1 siRNA reduced the expression of Bcl-xL, and negated survival promoting effect of BMP4. These data suggest that BMP4 promotes survival of NPCs by enhancing the anti-apoptotic function of Bcl-xL via BMP4-Smad1/5/8-Id1 signaling.
[Mh] Termos MeSH primário: Proteína Morfogenética Óssea 4/metabolismo
Fator 2 de Crescimento de Fibroblastos/metabolismo
Células-Tronco Neurais/metabolismo
Transdução de Sinais
Proteína bcl-X/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose
Diferenciação Celular
Proliferação Celular
Sobrevivência Celular
Células Cultivadas
Camundongos Endogâmicos C57BL
Células-Tronco Neurais/citologia
Regulação para Cima
Proteína bcl-X/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bcl2l1 protein, mouse); 0 (Bone Morphogenetic Protein 4); 0 (bcl-X Protein); 103107-01-3 (Fibroblast Growth Factor 2)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180122
[St] Status:MEDLINE


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[PMID]:29378551
[Au] Autor:Fu X; Li S; Zhou S; Wu Q; Jin F; Shi J
[Ad] Endereço:Joint International Research Laboratory of Ethnomedicine, Zunyi Medical College, Zunyi, Guizhou, China.
[Ti] Título:Stimulatory effect of icariin on the proliferation of neural stem cells from rat hippocampus.
[So] Source:BMC Complement Altern Med;18(1):34, 2018 Jan 29.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Icariin (ICA), a major ingredient of Epimediumbrevicornum, has various pharmacological activities including central nervous system protective functions such as the improvement of learning and memory function in mice models of Alzheimer's disease. It has been reported that ICA can promote regeneration of peripheral nerve and functional recovery. The purpose of this study was to investigate the potentiating effect of ICA on the proliferation of rat hippocampal neural stem cells, and explore the possible mechanism involved. METHODS: Primary neural stem cells were prepared from the hippocampus of newly born SD rats, and cells were cultured in special stem cell culture medium. Neural stem cells were confirmed by immunofluorescence detection of nestin, NSE and GFAP expression. The effect of ICA on the growth and proliferation of the neural stem cells was evaluated by 5-ethynyl-2-deoxyuridine (EdU) labeling of proliferating cells, and photomicrographic images of the cultured neural stem cells. Further, the mechanism of ICA-induced cell proliferation of neural stem cells was investigated by analyzing the gene and protein expression of cell cycle related genes cyclin D1 and p21. RESULTS: The present study showed that icariin promotes the growth and proliferation of neural stem cells from rat hippocampus in a dose-dependent manner. Incubation of cells with icariin resulted in significant increase in the number of stem cell spheres as well as the increased incorporation of EdU when compared with cells exposed to control vehicle. In addition, it was found that icariin-induced effect on neural stem cells is associated with increased mRNA and protein expression of cell cycle genes cyclin D1 and p21. CONCLUSIONS: This study evidently demonstrates the potentiating effect of ICA on neural stem cell growth and proliferation, which might be mediated through regulation of cell cycle gene and protein expression promoting cell cycle progression.
[Mh] Termos MeSH primário: Proliferação Celular/efeitos dos fármacos
Flavonoides/farmacologia
Hipocampo/citologia
Células-Tronco Neurais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Ciclina D1/metabolismo
Inibidor de Quinase Dependente de Ciclina p21/metabolismo
Células-Tronco Neurais/citologia
Células-Tronco Neurais/metabolismo
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (Flavonoids); 136601-57-5 (Cyclin D1); VNM47R2QSQ (icariin)
[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:180131
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-018-2095-y


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[PMID]:28451898
[Au] Autor:Liu XJ; Jiang X; Huang SN; Sun JY; Zhao F; Zeng WB; Luo MH
[Ad] Endereço:State Key Laboratory of Virology, CAS Center for Excellence in Brain Science and Intelligence Technology (CEBSIT), Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China.
[Ti] Título:Human cytomegalovirus infection dysregulates neural progenitor cell fate by disrupting Hes1 rhythm and down-regulating its expression.
[So] Source:Virol Sin;32(3):188-198, 2017 Jun.
[Is] ISSN:1995-820X
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:Human cytomegalovirus (HCMV) infection is a leading cause of birth defects, primarily affecting the central nervous system and causing its maldevelopment. As the essential downstream effector of Notch signaling pathway, Hes1, and its dynamic expression, plays an essential role on maintaining neural progenitor /stem cells (NPCs) cell fate and fetal brain development. In the present study, we reported the first observation of Hes1 oscillatory expression in human NPCs, with an approximately 1.5 hour periodicity and a Hes1 protein half-life of about 17 (17.6 ± 0.2) minutes. HCMV infection disrupts the Hes1 rhythm and down-regulates its expression. Furthermore, we discovered that depleting Hes1 protein disturbed NPCs cell fate by suppressing NPCs proliferation and neurosphere formation, and driving NPCs abnormal differentiation. These results suggested a novel mechanism linking disruption of Hes1 rhythm and down-regulation of Hes1 expression to neurodevelopmental disorders caused by congenital HCMV infection.
[Mh] Termos MeSH primário: Citomegalovirus/fisiologia
Interações Hospedeiro-Patógeno
Células-Tronco Neurais/fisiologia
Células-Tronco Neurais/virologia
Fatores de Transcrição HES-1/biossíntese
[Mh] Termos MeSH secundário: Diferenciação Celular
Proliferação Celular
Células Cultivadas
Regulação para Baixo
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Transcription Factor HES-1); 149348-15-2 (HES1 protein, human)
[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:170429
[St] Status:MEDLINE
[do] DOI:10.1007/s12250-017-3956-0


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[PMID]:29374155
[Au] Autor:Moon BS; Bai J; Cai M; Liu C; Shi J; Lu W
[Ad] Endereço:Department of Stem Cell Biology and Regenerative Medicine, Broad Center for Regenerative Medicine and Stem Cell Research, Keck School of Medicine, University of Southern California, Los Angeles, CA, 90033, USA.
[Ti] Título:Kruppel-like factor 4-dependent Staufen1-mediated mRNA decay regulates cortical neurogenesis.
[So] Source:Nat Commun;9(1):401, 2018 01 26.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Kruppel-like factor 4 (Klf4) is a zinc-finger-containing protein that plays a critical role in diverse cellular physiology. While most of these functions attribute to its role as a transcription factor, it is postulated that Klf4 may play a role other than transcriptional regulation. Here we demonstrate that Klf4 loss in neural progenitor cells (NPCs) leads to increased neurogenesis and reduced self-renewal in mice. In addition, Klf4 interacts with RNA-binding protein Staufen1 (Stau1) and RNA helicase Ddx5/17. They function together as a complex to maintain NPC self-renewal. We report that Klf4 promotes Stau1 recruitment to the 3'-untranslated region of neurogenesis-associated mRNAs, increasing Stau1-mediated mRNA decay (SMD) of these transcripts. Stau1 depletion abrogated SMD of target mRNAs and rescued neurogenesis defects in Klf4-overexpressing NPCs. Furthermore, Ddx5/17 knockdown significantly blocked Klf4-mediated mRNA degradation. Our results highlight a novel molecular mechanism underlying stability of neurogenesis-associated mRNAs controlled by the Klf4/Ddx5/17/Stau1 axis during mammalian corticogenesis.
[Mh] Termos MeSH primário: Córtex Cerebral/metabolismo
RNA Helicases DEAD-box/genética
Fatores de Transcrição Kruppel-Like/genética
Células-Tronco Neurais/metabolismo
Neurogênese/genética
RNA Mensageiro/genética
Proteínas de Ligação a RNA/genética
[Mh] Termos MeSH secundário: Animais
Proliferação Celular
Córtex Cerebral/citologia
Córtex Cerebral/crescimento & desenvolvimento
RNA Helicases DEAD-box/metabolismo
Embrião de Mamíferos
Feminino
Regulação da Expressão Gênica no Desenvolvimento
Células HEK293
Seres Humanos
Fatores de Transcrição Kruppel-Like/antagonistas & inibidores
Fatores de Transcrição Kruppel-Like/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Células-Tronco Neurais/citologia
Gravidez
Estabilidade de RNA
RNA Mensageiro/metabolismo
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Proteínas de Ligação a RNA/antagonistas & inibidores
Proteínas de Ligação a RNA/metabolismo
Proteínas de Ligação a RNA/toxicidade
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (GKLF protein); 0 (Kruppel-Like Transcription Factors); 0 (RNA, Messenger); 0 (RNA, Small Interfering); 0 (RNA-Binding Proteins); 0 (Stau1 protein, mouse); EC 3.6.1.- (Ddx17 protein, mouse); EC 3.6.1.- (Ddx5 protein, mouse); EC 3.6.4.13 (DEAD-box RNA Helicases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180128
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02720-9


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[PMID]:28453954
[Au] Autor:Pakulska MM; Tator CH; Shoichet MS
[Ad] Endereço:Department of Chemical Engineering and Applied Chemistry, University of Toronto, Toronto, ON, M5S 3E5, Canada; Institute for Biomaterials and Biomedical Engineering, University of Toronto, Toronto, ON, M5S 3G9, Canada.
[Ti] Título:Local delivery of chondroitinase ABC with or without stromal cell-derived factor 1α promotes functional repair in the injured rat spinal cord.
[So] Source:Biomaterials;134:13-21, 2017 Jul.
[Is] ISSN:1878-5905
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Traumatic spinal cord injury (SCI) is a devastating event for which functional recovery remains elusive. Due to the complex nature of SCI pathology, a combination treatment strategy will likely be required for success. We hypothesized that tissue and functional repair would be achieved in a rat model of impact-compression SCI by combining degradation of the glial scar, using chondroitinase ABC (ChABC), with recruitment of endogenous neural precursor cells (NPCs), using stromal cell-derived factor 1α (SDF). To test this hypothesis, we designed a crosslinked methylcellulose hydrogel (XMC) for minimally invasive, localized, and sustained intrathecal drug delivery. ChABC was released from XMC using protein-peptide affinity interactions while SDF was delivered by electrostatic affinity interactions from polymeric nanoparticles embedded in XMC. Rats with SCI were treated acutely with a combination of SDF and ChABC, SDF alone, ChABC alone, or vehicle alone, and compared to injury only. Treatment with ChABC, both alone and in combination with SDF, resulted in faster and more sustained behavioural improvement over time than other groups. The significantly reduced chondroitin sulfate proteoglycan levels and greater distribution of NPCs throughout the spinal cord tissue with ChABC delivery, both alone and in combination with SDF, may explain the improved locomotor function. Treatment with SDF alone had no apparent effect on NPC number or distribution nor synergistic effect with ChABC delivery. Thus, in this model of SCI, tissue and functional repair is attributed to ChABC.
[Mh] Termos MeSH primário: Quimiocina CXCL12/química
Condroitina ABC Liase/metabolismo
Traumatismos da Medula Espinal/metabolismo
[Mh] Termos MeSH secundário: Animais
Quimiocina CXCL12/metabolismo
Quimiocina CXCL12/uso terapêutico
Condroitina ABC Liase/química
Proteoglicanas de Sulfatos de Condroitina/química
Ensaio de Imunoadsorção Enzimática
Feminino
Hidrogel de Polietilenoglicol-Dimetacrilato/química
Imuno-Histoquímica
Metilcelulose/química
Células-Tronco Neurais/citologia
Células-Tronco Neurais/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Traumatismos da Medula Espinal/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL12); 0 (Chondroitin Sulfate Proteoglycans); 25852-47-5 (Hydrogel, Polyethylene Glycol Dimethacrylate); 9004-67-5 (Methylcellulose); EC 4.2.2.20 (Chondroitin ABC Lyase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


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[PMID]:28471118
[Au] Autor:Dong J; Zhu G; Wang TC; Shi FS
[Ad] Endereço:Department of Veterinary Medicine, College of Animal Sciences, Zhejiang University, Hangzhou 310058, China.
[Ti] Título:Ginsenoside Rg1 promotes neural differentiation of mouse adipose-derived stem cells via the miRNA-124 signaling pathway.
[So] Source:J Zhejiang Univ Sci B;18(5):445-448, 2017 May.
[Is] ISSN:1862-1783
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:We have explored the role of ginsenoside Rg1 in promoting the differentiation of mouse adipose-derived stem cells (mADSC) towards the neuronal lineage. The central nervous system has long been regarded as incapable of self-repair; therefore neuronal differentiation from stem cells is of great interest. However, the use of embryonic stem cells is limited due to their inaccessibility and for ethical reasons, so the search is on for alternative pluripotent cells capable of differentiating into neuronal cells. Adipose-derived stem cells (ADSC) can differentiate into different cell types, including neuronal cells: their accessibility, low risk, and capacity for long-term growth and self-renewal have made them the preferred stem cell type for clinical applications. Several methods have been indicated for promoting the neuronal differentiation of ADSC, but the mechanism of this process has not been clearly identified. As our previous study showed that microRNA-124 (miRNA-124) plays a positive role in promoting the neural differentiation of ADSC, we wanted to find reagents that can upregulate miRNA-124 expression during neural differentiation.
[Mh] Termos MeSH primário: Ginsenosídeos/administração & dosagem
MicroRNAs/metabolismo
Células-Tronco Neurais/efeitos dos fármacos
Células-Tronco Neurais/fisiologia
Neurogênese/fisiologia
Neurônios/fisiologia
[Mh] Termos MeSH secundário: Adipócitos/citologia
Adipócitos/fisiologia
Animais
Diferenciação Celular/efeitos dos fármacos
Diferenciação Celular/fisiologia
Células Cultivadas
Relação Dose-Resposta a Droga
Camundongos
Células-Tronco Neurais/citologia
Neurogênese/efeitos dos fármacos
Neurônios/citologia
Neurônios/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ginsenosides); 0 (MicroRNAs); 0 (Mirn124 microRNA, mouse); PJ788634QY (ginsenoside Rg1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1631/jzus.B1600355


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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]:29338033
[Au] Autor:Dreyer-Andersen N; Almeida AS; Jensen P; Kamand M; Okarmus J; Rosenberg T; Friis SD; Martínez Serrano A; Blaabjerg M; Kristensen BW; Skrydstrup T; Gramsbergen JB; Vieira HLA; Meyer M
[Ad] Endereço:Department of Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark.
[Ti] Título:Intermittent, low dose carbon monoxide exposure enhances survival and dopaminergic differentiation of human neural stem cells.
[So] Source:PLoS One;13(1):e0191207, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Exploratory studies using human fetal tissue have suggested that intrastriatal transplantation of dopaminergic neurons may become a future treatment for patients with Parkinson's disease. However, the use of human fetal tissue is compromised by ethical, regulatory and practical concerns. Human stem cells constitute an alternative source of cells for transplantation in Parkinson's disease, but efficient protocols for controlled dopaminergic differentiation need to be developed. Short-term, low-level carbon monoxide (CO) exposure has been shown to affect signaling in several tissues, resulting in both protection and generation of reactive oxygen species. The present study investigated the effect of CO produced by a novel CO-releasing molecule on dopaminergic differentiation of human neural stem cells. Short-term exposure to 25 ppm CO at days 0 and 4 significantly increased the relative content of ß-tubulin III-immunoreactive immature neurons and tyrosine hydroxylase expressing catecholaminergic neurons, as assessed 6 days after differentiation. Also the number of microtubule associated protein 2-positive mature neurons had increased significantly. Moreover, the content of apoptotic cells (Caspase3) was reduced, whereas the expression of a cell proliferation marker (Ki67) was left unchanged. Increased expression of hypoxia inducible factor-1α and production of reactive oxygen species (ROS) in cultures exposed to CO may suggest a mechanism involving mitochondrial alterations and generation of ROS. In conclusion, the present procedure using controlled, short-term CO exposure allows efficient dopaminergic differentiation of human neural stem cells at low cost and may as such be useful for derivation of cells for experimental studies and future development of donor cells for transplantation in Parkinson's disease.
[Mh] Termos MeSH primário: Monóxido de Carbono/administração & dosagem
Células-Tronco Neurais/citologia
Células-Tronco Neurais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Monóxido de Carbono/metabolismo
Diferenciação Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Citocinas/metabolismo
Neurônios Dopaminérgicos/citologia
Neurônios Dopaminérgicos/efeitos dos fármacos
Neurônios Dopaminérgicos/metabolismo
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Células-Tronco Neurais/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Silanos/administração & dosagem
Silanos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (HIF1A protein, human); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Reactive Oxygen Species); 0 (Silanes); 7U1EE4V452 (Carbon Monoxide)
[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:180117
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191207


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[PMID]:28450582
[Au] Autor:McConnell MJ; Moran JV; Abyzov A; Akbarian S; Bae T; Cortes-Ciriano I; Erwin JA; Fasching L; Flasch DA; Freed D; Ganz J; Jaffe AE; Kwan KY; Kwon M; Lodato MA; Mills RE; Paquola ACM; Rodin RE; Rosenbluh C; Sestan N; Sherman MA; Shin JH; Song S; Straub RE; Thorpe J; Weinberger DR; Urban AE; Zhou B; Gage FH; Lehner T; Senthil G; Walsh CA; Chess A; Courchesne E; Gleeson JG; Kidd JM; Park PJ; Pevsner J; Vaccarino FM; Brain Somatic Mosaicism Network
[Ti] Título:Intersection of diverse neuronal genomes and neuropsychiatric disease: The Brain Somatic Mosaicism Network.
[So] Source:Science;356(6336), 2017 Apr 28.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neuropsychiatric disorders have a complex genetic architecture. Human genetic population-based studies have identified numerous heritable sequence and structural genomic variants associated with susceptibility to neuropsychiatric disease. However, these germline variants do not fully account for disease risk. During brain development, progenitor cells undergo billions of cell divisions to generate the ~80 billion neurons in the brain. The failure to accurately repair DNA damage arising during replication, transcription, and cellular metabolism amid this dramatic cellular expansion can lead to somatic mutations. Somatic mutations that alter subsets of neuronal transcriptomes and proteomes can, in turn, affect cell proliferation and survival and lead to neurodevelopmental disorders. The long life span of individual neurons and the direct relationship between neural circuits and behavior suggest that somatic mutations in small populations of neurons can significantly affect individual neurodevelopment. The Brain Somatic Mosaicism Network has been founded to study somatic mosaicism both in neurotypical human brains and in the context of complex neuropsychiatric disorders.
[Mh] Termos MeSH primário: Encéfalo/anormalidades
Transtornos Mentais/genética
Mosaicismo
Doenças do Sistema Nervoso/genética
Células-Tronco Neurais/fisiologia
Neurônios/fisiologia
[Mh] Termos MeSH secundário: Encéfalo/metabolismo
Divisão Celular/genética
Dano ao DNA
Análise Mutacional de DNA/métodos
Reparo do DNA/genética
Replicação do DNA
Genoma Humano
Células Germinativas/metabolismo
Seres Humanos
Rede Nervosa/crescimento & desenvolvimento
Rede Nervosa/metabolismo
Células-Tronco Neurais/metabolismo
Neurônios/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[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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