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Pesquisa : A11.284.180.075.249 [Categoria DeCS]
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[PMID]:29370308
[Au] Autor:Zhang M; Zhou Q; Luo Y; Nguyen T; Rosenblatt MI; Guaiquil VH
[Ad] Endereço:Department of Ophthalmology and Visual Sciences, University of Illinois-Chicago, Chicago, Illinois, United States of America.
[Ti] Título:Semaphorin3A induces nerve regeneration in the adult cornea-a switch from its repulsive role in development.
[So] Source:PLoS One;13(1):e0191962, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The peripheral sensory nerves that innervate the cornea can be easily damaged by trauma, surgery, infection or diabetes. Several growth factors and axon guidance molecules, such as Semaphorin3A (Sema3A) are upregulated upon cornea injury. Nerves can regenerate after injury but do not recover their original density and patterning. Sema3A is a well known axon guidance and growth cone repellent protein during development, however its role in adult cornea nerve regeneration remains undetermined. Here we investigated the neuro-regenerative potential of Sema3A on adult peripheral nervous system neurons such as those that innervate the cornea. First, we examined the gene expression profile of the Semaphorin class 3 family members and found that all are expressed in the cornea. However, upon cornea injury there is a fast increase in Sema3A expression. We then corroborated that Sema3A totally abolished the growth promoting effect of nerve growth factor (NGF) on embryonic neurons and observed signs of growth cone collapse and axonal retraction after 30 min of Sema3A addition. However, in adult isolated trigeminal ganglia or dorsal root ganglia neurons, Sema3A did not inhibited the NGF-induced neuronal growth. Furthermore, adult neurons treated with Sema3A alone produced similar neuronal growth to cells treated with NGF and the length of the neurites and branching was comparable between both treatments. These effects were replicated in vivo, where thy1-YFP neurofluorescent mice subjected to cornea epithelium debridement and receiving intrastromal pellet implantation containing Sema3A showed increased corneal nerve regeneration than those receiving pellets with vehicle. In adult PNS neurons, Sema3A is a potent inducer of neuronal growth in vitro and cornea nerve regeneration in vivo. Our data indicates a functional switch for the role of Sema3A in PNS neurons where the well-described repulsive role during development changes to a growth promoting effect during adulthood. The high expression of Sema3A in the normal and injured adult corneas could be related to its role as a growth factor.
[Mh] Termos MeSH primário: Regeneração Nervosa/efeitos dos fármacos
Semaforina-3A/farmacologia
[Mh] Termos MeSH secundário: Animais
Epitélio Anterior/efeitos dos fármacos
Epitélio Anterior/lesões
Epitélio Anterior/metabolismo
Gânglios Espinais/citologia
Gânglios Espinais/efeitos dos fármacos
Cones de Crescimento/efeitos dos fármacos
Camundongos
Nervo Trigêmeo/citologia
Nervo Trigêmeo/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Semaphorin-3A)
[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:180126
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191962


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[PMID]:28844905
[Au] Autor:Wang J; Pavlyk I; Vedula P; Sterling S; Leu NA; Dong DW; Kashina A
[Ad] Endereço:University of Pennsylvania, School of Veterinary Medicine, Philadelphia, PA 19104, United States.
[Ti] Título:Arginyltransferase ATE1 is targeted to the neuronal growth cones and regulates neurite outgrowth during brain development.
[So] Source:Dev Biol;430(1):41-51, 2017 10 01.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Arginylation is an emerging protein modification mediated by arginyltransferase ATE1, shown to regulate embryogenesis and actin cytoskeleton, however its functions in different physiological systems are not well understood. Here we analyzed the role of ATE1 in brain development and neuronal growth by producing a conditional mouse knockout with Ate1 deletion in the nervous system driven by Nestin promoter (Nes-Ate1 mice). These mice were weaker than wild type, resulting in low postnatal survival rates, and had abnormalities in the brain that suggested defects in neuronal migration. Cultured Ate1 knockout neurons showed a reduction in the neurite outgrowth and the levels of doublecortin and F-actin in the growth cones. In wild type, ATE1 prominently localized to the growth cones, in addition to the cell bodies. Examination of the Ate1 mRNA sequence reveals the existence of putative zipcode-binding sequences involved in mRNA targeting to the cell periphery and local translation at the growth cones. Fluorescence in situ hybridization showed that Ate1 mRNA localized to the tips of the growth cones, likely due to zipcode-mediated targeting, and this localization coincided with spots of localization of arginylated ß-actin, which disappeared in the presence of protein synthesis inhibitors. We propose that zipcode-mediated co-targeting of Ate1 and ß-actin mRNA leads to localized co-translational arginylation of ß-actin that drives the growth cone migration and neurite outgrowth.
[Mh] Termos MeSH primário: Aminoaciltransferases/metabolismo
Encéfalo/crescimento & desenvolvimento
Encéfalo/metabolismo
Cones de Crescimento/enzimologia
Neuritos/enzimologia
Crescimento Neuronal
[Mh] Termos MeSH secundário: Actinas/metabolismo
Animais
Arginina/metabolismo
Encéfalo/anormalidades
Encéfalo/patologia
Movimento Celular
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Proteínas Associadas aos Microtúbulos/metabolismo
Modelos Biológicos
Neuropeptídeos/metabolismo
Biossíntese de Proteínas
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Actins); 0 (Microtubule-Associated Proteins); 0 (Neuropeptides); 0 (RNA, Messenger); 0 (doublecortin protein); 94ZLA3W45F (Arginine); EC 2.3.2.- (Aminoacyltransferases); EC 2.3.2.8 (arginyltransferase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170829
[St] Status:MEDLINE


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[PMID]:28772118
[Au] Autor:Bendriem RM; Ross ME
[Ad] Endereço:Feil Family Brain and Mind Research Institute and Center for Neurogenetics, Weill Cornell Medicine, New York, NY 10021, USA.
[Ti] Título:Wiring the Human Brain: A User's Handbook.
[So] Source:Neuron;95(3):482-485, 2017 Aug 02.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Brain function requires connecting neuronal networks to empower movement, sensation, behavior, and cognition. Studies published early this year provide evidence that in humans, Netrin receptor, Deleted in Colorectal Cancer (DCC), is a master regulator of axonal crossing throughout the neuraxis.
[Mh] Termos MeSH primário: Axônios/fisiologia
Encéfalo/metabolismo
Cones de Crescimento/fisiologia
Fatores de Crescimento Neural/metabolismo
Neurônios/fisiologia
Receptores de Superfície Celular/metabolismo
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Receptores de Netrina
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Nerve Growth Factors); 0 (Netrin Receptors); 0 (Receptors, Cell Surface)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE


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[PMID]:28652571
[Au] Autor:Takano T; Wu M; Nakamuta S; Naoki H; Ishizawa N; Namba T; Watanabe T; Xu C; Hamaguchi T; Yura Y; Amano M; Hahn KM; Kaibuchi K
[Ad] Endereço:Department of Cell Pharmacology, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
[Ti] Título:Discovery of long-range inhibitory signaling to ensure single axon formation.
[So] Source:Nat Commun;8(1):33, 2017 06 26.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A long-standing question in neurodevelopment is how neurons develop a single axon and multiple dendrites from common immature neurites. Long-range inhibitory signaling from the growing axon is hypothesized to prevent outgrowth of other immature neurites and to differentiate them into dendrites, but the existence and nature of this inhibitory signaling remains unknown. Here, we demonstrate that axonal growth triggered by neurotrophin-3 remotely inhibits neurite outgrowth through long-range Ca waves, which are delivered from the growing axon to the cell body. These Ca waves increase RhoA activity in the cell body through calcium/calmodulin-dependent protein kinase I. Optogenetic control of Rho-kinase combined with computational modeling reveals that active Rho-kinase diffuses to growing other immature neurites and inhibits their outgrowth. Mechanistically, calmodulin-dependent protein kinase I phosphorylates a RhoA-specific GEF, GEF-H1, whose phosphorylation enhances its GEF activity. Thus, our results reveal that long-range inhibitory signaling mediated by Ca wave is responsible for neuronal polarization.Emerging evidence suggests that gut microbiota influences immune function in the brain and may play a role in neurological diseases. Here, the authors offer in vivo evidence from a Drosophila model that supports a role for gut microbiota in modulating the progression of Alzheimer's disease.
[Mh] Termos MeSH primário: Segmento Inicial do Axônio/metabolismo
Sinalização do Cálcio
Cálcio/metabolismo
Cones de Crescimento/metabolismo
Neuritos/metabolismo
Proteínas rho de Ligação ao GTP/genética
[Mh] Termos MeSH secundário: Animais
Segmento Inicial do Axônio/ultraestrutura
Proteína Quinase Tipo 1 Dependente de Cálcio-Calmodulina/genética
Proteína Quinase Tipo 1 Dependente de Cálcio-Calmodulina/metabolismo
Comunicação Celular
Diferenciação Celular
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Embrião de Mamíferos
Regulação da Expressão Gênica no Desenvolvimento
Cones de Crescimento/ultraestrutura
Hipocampo/citologia
Hipocampo/crescimento & desenvolvimento
Hipocampo/metabolismo
Camundongos
Camundongos Endogâmicos ICR
Fatores de Crescimento Neural/genética
Fatores de Crescimento Neural/metabolismo
Fatores de Crescimento Neural/farmacologia
Neuritos/ultraestrutura
Neurogênese/genética
Imagem Óptica
Optogenética
Cultura Primária de Células
Transporte Proteico
Fatores de Troca de Nucleotídeo Guanina Rho/genética
Fatores de Troca de Nucleotídeo Guanina Rho/metabolismo
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
Proteínas rho de Ligação ao GTP/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 (Arhgef2 protein, mouse); 0 (DNA-Binding Proteins); 0 (GLUT4 enhancer factor, mouse); 0 (Nerve Growth Factors); 0 (Rho Guanine Nucleotide Exchange Factors); 0 (Transcription Factors); 0 (neurotropin 3, mouse); EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 1); EC 3.6.5.2 (RhoA protein, mouse); EC 3.6.5.2 (rho GTP-Binding Proteins); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170628
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-00044-2


  5 / 2489 MEDLINE  
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[PMID]:28472086
[Au] Autor:Yap YC; King AE; Guijt RM; Jiang T; Blizzard CA; Breadmore MC; Dickson TC
[Ad] Endereço:Menzies Institute for Medical Research, University of Tasmania, Tasmania, Australia.
[Ti] Título:Mild and repetitive very mild axonal stretch injury triggers cystoskeletal mislocalization and growth cone collapse.
[So] Source:PLoS One;12(5):e0176997, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Diffuse axonal injury is a hallmark pathological consequence of non-penetrative traumatic brain injury (TBI) and yet the axonal responses to stretch injury are not fully understood at the cellular level. Here, we investigated the effects of mild (5%), very mild (0.5%) and repetitive very mild (2×0.5%) axonal stretch injury on primary cortical neurons using a recently developed compartmentalized in vitro model. We found that very mild and mild levels of stretch injury resulted in the formation of smaller growth cones at the tips of axons and a significantly higher number of collapsed structures compared to those present in uninjured cultures, when measured at both 24 h and 72 h post injury. Immunocytochemistry studies revealed that at 72 h following mild injury the axonal growth cones had a significantly higher colocalization of ßIII tubulin and F-actin and higher percentage of collapsed morphology than those present following a very mild injury. Interestingly, cultures that received a second very mild stretch injury, 24 h after the first insult, had a further increased proportion of growth cone collapse and increased ßIII tubulin and F-actin colocalization, compared with a single very mild injury at 72 h PI. In addition, our results demonstrated that microtubule stabilization of axons using brain penetrant Epothilone D (EpoD) (100 nM) resulted in a significant reduction in the number of fragmented axons following mild injury. Collectively, these results suggest that mild and very mild stretch injury to a very localized region of the cortical axon is able to trigger a degenerative response characterized by growth cone collapse and significant abnormal cytoskeletal rearrangement. Furthermore, repetitive very mild stretch injury significantly exacerbated this response. Results suggest that axonal degeneration following stretch injury involves destabilization of the microtubule cytoskeleton and hence treatment with EpoD reduced fragmentation. Together, these results contribute a better understanding of the pathogenesis of mild and repetitive TBI and highlight the therapeutic effect of microtubule targeted drugs on distal part of neurons using a compartmentalized culturing model.
[Mh] Termos MeSH primário: Axônios
Citoesqueleto/metabolismo
Lesão Axonal Difusa/patologia
Cones de Crescimento/patologia
[Mh] Termos MeSH secundário: Células Cultivadas
Seres Humanos
Técnicas In Vitro
Microfluídica/instrumentação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0176997


  6 / 2489 MEDLINE  
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[PMID]:28445456
[Au] Autor:Dominici C; Moreno-Bravo JA; Puiggros SR; Rappeneau Q; Rama N; Vieugue P; Bernet A; Mehlen P; Chédotal A
[Ad] Endereço:Sorbonne Universités, UPMC Univ Paris 06, INSERM, CNRS, Institut de la Vision, 17 Rue Moreau, 75012 Paris, France.
[Ti] Título:Floor-plate-derived netrin-1 is dispensable for commissural axon guidance.
[So] Source:Nature;545(7654):350-354, 2017 05 18.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Netrin-1 is an evolutionarily conserved, secreted extracellular matrix protein involved in axon guidance at the central nervous system midline. Netrin-1 is expressed by cells localized at the central nervous system midline, such as those of the floor plate in vertebrate embryos. Growth cone turning assays and three-dimensional gel diffusion assays have shown that netrin-1 can attract commissural axons. Loss-of-function experiments further demonstrated that commissural axon extension to the midline is severely impaired in the absence of netrin-1 (refs 3, 7, 8, 9). Together, these data have long supported a model in which commissural axons are attracted by a netrin-1 gradient diffusing from the midline. Here we selectively ablate netrin-1 expression in floor-plate cells using a Ntn1 conditional knockout mouse line. We find that hindbrain and spinal cord commissural axons develop normally in the absence of floor-plate-derived netrin-1. Furthermore, we show that netrin-1 is highly expressed by cells in the ventricular zone, which can release netrin-1 at the pial surface where it binds to commissural axons. Notably, Ntn1 deletion from the ventricular zone phenocopies commissural axon guidance defects previously described in Ntn1-knockout mice. These results show that the classical view that attraction of commissural axons is mediated by a gradient of floor-plate-derived netrin-1 is inaccurate and that netrin-1 primarily acts locally by promoting growth cone adhesion.
[Mh] Termos MeSH primário: Orientação de Axônios
Cones de Crescimento/metabolismo
Fatores de Crescimento Neural/metabolismo
Fatores de Crescimento Neural/secreção
Medula Espinal/citologia
Proteínas Supressoras de Tumor/metabolismo
Proteínas Supressoras de Tumor/secreção
[Mh] Termos MeSH secundário: Animais
Adesão Celular
Feminino
Masculino
Camundongos
Camundongos Knockout
Fatores de Crescimento Neural/deficiência
Netrina-1
Células-Tronco Neurais/citologia
Células-Tronco Neurais/metabolismo
Proteínas Supressoras de Tumor/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Nerve Growth Factors); 0 (Ntn1 protein, mouse); 0 (Tumor Suppressor Proteins); 158651-98-0 (Netrin-1)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1038/nature22331


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[PMID]:28356421
[Au] Autor:Iizuka Y; Mooneyham A; Sieben A; Chen K; Maile M; Hellweg R; Schütz F; Teckle K; Starr T; Thayanithy V; Vogel RI; Lou E; Lee MK; Bazzaro M
[Ad] Endereço:Masonic Cancer Center and Department of Obstetrics, Gynecology and Women's Heath, University of Minnesota Twin Cities, Minneapolis, MN 55455.
[Ti] Título:UNC-45A is required for neurite extension via controlling NMII activation.
[So] Source:Mol Biol Cell;28(10):1337-1346, 2017 May 15.
[Is] ISSN:1939-4586
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNC-45A is a highly conserved member of the UNC-45/CRO1/She4p family of proteins, which act as chaperones for conventional and nonconventional myosins. NMII mediates contractility and actin-based motility, which are fundamental for proper growth cone motility and neurite extension. The presence and role of UNC-45A in neuronal differentiation have been largely unknown. Here we demonstrate that UNC-45A is a novel growth cone--localized, NMII-associated component of the multiprotein complex regulating growth cone dynamics. We show that UNC-45A is dispensable for neuron survival but required for neurite elongation. Mechanistically, loss of UNC-45A results in increased levels of NMII activation. Collectively our results provide novel insights into the molecular mechanisms of neurite growth and define UNC-45A as a novel and master regulator of NMII-mediated cellular processes in neurons.
[Mh] Termos MeSH primário: Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
[Mh] Termos MeSH secundário: Actinas/metabolismo
Animais
Linhagem Celular
Movimento Celular/fisiologia
Cones de Crescimento/metabolismo
Seres Humanos
Peptídeos e Proteínas de Sinalização Intracelular/fisiologia
Camundongos
Chaperonas Moleculares/metabolismo
Proteínas Motores Moleculares/metabolismo
Cadeias Pesadas de Miosina/metabolismo
Miosinas/metabolismo
Neuritos/metabolismo
Neurônios/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Intracellular Signaling Peptides and Proteins); 0 (MYH9 protein, human); 0 (Molecular Chaperones); 0 (Molecular Motor Proteins); 0 (UNC45A protein, human); EC 3.6.4.1 (Myosin Heavy Chains); EC 3.6.4.1 (Myosins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170331
[St] Status:MEDLINE
[do] DOI:10.1091/mbc.E16-06-0381


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[PMID]:28320840
[Au] Autor:Huang CY; Lien CC; Cheng CF; Yen TY; Chen CJ; Tsaur ML
[Ad] Endereço:Institute of Neuroscience, Brain Research Center, National Yang-Ming University, Taipei 112, Taiwan.
[Ti] Título:K Channel Kv3.4 Is Essential for Axon Growth by Limiting the Influx of Ca into Growth Cones.
[So] Source:J Neurosci;37(17):4433-4449, 2017 Apr 26.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Membrane excitability in the axonal growth cones of embryonic neurons influences axon growth. Voltage-gated K (Kv) channels are key factors in controlling membrane excitability, but whether they regulate axon growth remains unclear. Here, we report that Kv3.4 is expressed in the axonal growth cones of embryonic spinal commissural neurons, motoneurons, dorsal root ganglion neurons, retinal ganglion cells, and callosal projection neurons during axon growth. Our (cultured dorsal spinal neurons of chick embryos) and (developing chick spinal commissural axons and rat callosal axons) findings demonstrate that knockdown of Kv3.4 by a specific shRNA impedes axon initiation, elongation, pathfinding, and fasciculation. In cultured dorsal spinal neurons, blockade of Kv3.4 by blood depressing substance II suppresses axon growth via an increase in the amplitude and frequency of Ca influx through T-type and L-type Ca channels. Electrophysiological results show that Kv3.4, the major Kv channel in the axonal growth cones of embryonic dorsal spinal neurons, is activated at more hyperpolarized potentials and inactivated more slowly than it is in postnatal and adult neurons. The opening of Kv3.4 channels effectively reduces growth cone membrane excitability, thereby limiting excessive Ca influx at subthreshold potentials or during Ca -dependent action potentials. Furthermore, excessive Ca influx induced by an optogenetic approach also inhibits axon growth. Our findings suggest that Kv3.4 reduces growth cone membrane excitability and maintains [Ca ] at an optimal concentration for normal axon growth. Accumulating evidence supports the idea that impairments in axon growth contribute to many clinical disorders, such as autism spectrum disorders, corpus callosum agenesis, Joubert syndrome, Kallmann syndrome, and horizontal gaze palsy with progressive scoliosis. Membrane excitability in the growth cone, which is mainly controlled by voltage-gated Ca (Cav) and K (Kv) channels, modulates axon growth. The role of Cav channels during axon growth is well understood, but it is unclear whether Kv channels control axon outgrowth by regulating Ca influx. This report shows that Kv3.4, which is transiently expressed in the axonal growth cones of many types of embryonic neurons, acts to reduce excessive Ca influx through Cav channels and thus permits normal axon outgrowth.
[Mh] Termos MeSH primário: Axônios/fisiologia
Cálcio/metabolismo
Cones de Crescimento/metabolismo
Canais de Potássio de Abertura Dependente da Tensão da Membrana/metabolismo
[Mh] Termos MeSH secundário: Potenciais de Ação/fisiologia
Animais
Embrião de Galinha
Corpo Caloso/citologia
Corpo Caloso/metabolismo
Eletroporação
Gânglios Espinais/citologia
Gânglios Espinais/metabolismo
Técnicas de Silenciamento de Genes
Neurônios Motores/metabolismo
Neurônios/metabolismo
Canais de Potássio de Abertura Dependente da Tensão da Membrana/genética
Ratos
Células Ganglionares da Retina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Potassium Channels, Voltage-Gated); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.1076-16.2017


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[PMID]:28246119
[Au] Autor:Moradi M; Sivadasan R; Saal L; Lüningschrör P; Dombert B; Rathod RJ; Dieterich DC; Blum R; Sendtner M
[Ad] Endereço:Institute of Clinical Neurobiology, University Hospital Wuerzburg, University of Wuerzburg, 97078 Wuerzburg, Germany.
[Ti] Título:Differential roles of α-, ß-, and γ-actin in axon growth and collateral branch formation in motoneurons.
[So] Source:J Cell Biol;216(3):793-814, 2017 Mar 06.
[Is] ISSN:1540-8140
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Axonal branching and terminal arborization are fundamental events during the establishment of synaptic connectivity. They are triggered by assembly of actin filaments along axon shafts giving rise to filopodia. The specific contribution of the three actin isoforms, Actα, Actß, and Actγ, to filopodia stability and dynamics during this process is not well understood. Here, we report that Actα, Actß, and Actγ isoforms are expressed in primary mouse motoneurons and their transcripts are translocated into axons. shRNA-mediated depletion of Actα reduces axonal filopodia dynamics and disturbs collateral branch formation. Knockdown of Actß reduces dynamic movements of growth cone filopodia and impairs presynaptic differentiation. Ablation of Actß or Actγ leads to compensatory up-regulation of the two other isoforms, which allows maintenance of total actin levels and preserves F-actin polymerization. Collectively, our data provide evidence for specific roles of different actin isoforms in spatial regulation of actin dynamics and stability in axons of developing motoneurons.
[Mh] Termos MeSH primário: Actinas/metabolismo
Axônios/metabolismo
Neurônios Motores/metabolismo
[Mh] Termos MeSH secundário: Citoesqueleto de Actina/metabolismo
Animais
Células Cultivadas
Cones de Crescimento/metabolismo
Camundongos
Fator de Crescimento Neural/metabolismo
Neurogênese/fisiologia
Pseudópodes/metabolismo
Células Receptoras Sensoriais
Regulação para Cima/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 9061-61-4 (Nerve Growth Factor)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170302
[St] Status:MEDLINE
[do] DOI:10.1083/jcb.201604117


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[PMID]:28238735
[Au] Autor:Craft TR; Forrester WC
[Ad] Endereço:Medical Sciences Program, Indiana University, Bloomington, IN 47405, United States.
[Ti] Título:The Caenorhabditis elegans matrix non-peptidase MNP-1 is required for neuronal cell migration and interacts with the Ror receptor tyrosine kinase CAM-1.
[So] Source:Dev Biol;424(1):18-27, 2017 04 01.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Directed cell migration is critical for metazoan development. During Caenorhabditis elegans development many neuronal, muscle and other cell types migrate. Multiple classes of proteins have been implicated in cell migration including secreted guidance cues, receptors for guidance cues and intracellular proteins that respond to cues to polarize cells and produce the forces that move them. In addition, cell surface and secreted proteases have been identified that may clear the migratory route and process guidance cues. We report here that mnp-1 is required for neuronal cell and growth cone migrations. MNP-1 is expressed by migrating cells and functions cell autonomously for cell migrations. We also find a genetic interaction between mnp-1 and cam-1, which encodes a Ror receptor tyrosine kinase required for some of the same cell migrations.
[Mh] Termos MeSH primário: Proteínas de Caenorhabditis elegans/metabolismo
Caenorhabditis elegans/citologia
Caenorhabditis elegans/enzimologia
Movimento Celular
Neurônios/citologia
Neurônios/enzimologia
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/metabolismo
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Proteínas de Caenorhabditis elegans/química
Proteínas de Caenorhabditis elegans/genética
Linhagem da Célula
Cones de Crescimento/metabolismo
Músculos/citologia
Mutação/genética
Especificidade de Órgãos
Ligação Proteica
Fatores de Transcrição/química
Fatores de Transcrição/genética
Transgenes
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Caenorhabditis elegans Proteins); 0 (MNP-1 protein, C elegans); 0 (Transcription Factors); EC 2.7.10.1 (CAM-1 protein, C elegans); EC 2.7.10.1 (Receptor Tyrosine Kinase-like Orphan Receptors)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170228
[St] Status:MEDLINE



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