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Pesquisa : G11.561.585.250 [Categoria DeCS]
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[PMID]:28456003
[Au] Autor:Röhr D; Halfter H; Schulz JB; Young P; Gess B
[Ad] Endereço:Department of Sleep Medicine and Neuromuscular Disorders, University Hospital Muenster, Muenster, Germany.
[Ti] Título:Sodium-dependent Vitamin C transporter 2 deficiency impairs myelination and remyelination after injury: Roles of collagen and demethylation.
[So] Source:Glia;65(7):1186-1200, 2017 Jul.
[Is] ISSN:1098-1136
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Peripheral nerve myelination involves rapid production of tightly bound lipid layers requiring cholesterol biosynthesis and myelin protein expression, but also a collagen-containing extracellular matrix providing mechanical stability. In previous studies, we showed a function of ascorbic acid in peripheral nerve myelination and extracellular matrix formation in adult mice. Here, we sought the mechanism of action of ascorbic acid in peripheral nerve myelination using different paradigms of myelination in vivo and in vitro. We found impaired myelination and reduced collagen expression in Sodium-dependent Vitamin C Transporter 2 heterozygous mice (SVCT2 ) during peripheral nerve development and after peripheral nerve injury. In dorsal root ganglion (DRG) explant cultures, hypo-myelination could be rescued by precoating with different collagen types. The activity of the ascorbic acid-dependent demethylating Ten-eleven-translocation (Tet) enzymes was reduced in ascorbic acid deprived and SVCT2 DRG cultures. Further, in ascorbic acid-deprived DRG cultures, methylation of a CpG island in the collagen alpha1 (IV) and alpha2 (IV) bidirectional promoter region was increased compared to wild-type and ascorbic acid treated controls. Taken together, these results provide further evidence for the function of ascorbic acid in myelination and extracellular matrix formation in peripheral nerves and suggest a putative molecular mechanism of ascorbic acid function in Tet-dependent demethylation of collagen promoters.
[Mh] Termos MeSH primário: Colágeno/metabolismo
Desmetilação
Traumatismos dos Nervos Periféricos/genética
Traumatismos dos Nervos Periféricos/fisiopatologia
Remielinização/genética
Transportadores de Sódio Acoplados à Vitamina C/deficiência
[Mh] Termos MeSH secundário: Animais
Ácido Ascórbico/farmacologia
Células Cultivadas
Colágeno/genética
Modelos Animais de Doenças
Feminino
Transtornos Neurológicos da Marcha/etiologia
Gânglios Espinais/citologia
Masculino
Camundongos
Camundongos Transgênicos
Nervos Periféricos/patologia
Nervos Periféricos/ultraestrutura
RNA Mensageiro/metabolismo
Teste de Desempenho do Rota-Rod
Células Receptoras Sensoriais/metabolismo
Células Receptoras Sensoriais/patologia
Transportadores de Sódio Acoplados à Vitamina C/genética
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (Slc23a2 protein, mouse); 0 (Sodium-Coupled Vitamin C Transporters); 9007-34-5 (Collagen); PQ6CK8PD0R (Ascorbic Acid)
[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.23152


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[PMID]:28451635
[Au] Autor:Moyon S; Ma D; Huynh JL; Coutts DJC; Zhao C; Casaccia P; Franklin RJM
[Ad] Endereço:Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
[Ti] Título:Efficient Remyelination Requires DNA Methylation.
[So] Source:eNeuro;4(2), 2017 Mar-Apr.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oligodendrocyte progenitor cells (OPCs) are the principal source of new myelin in the central nervous system. A better understanding of how they mature into myelin-forming cells is of high relevance for remyelination. It has recently been demonstrated that during developmental myelination, the DNA methyltransferase 1 (DNMT1), but not DNMT3A, is critical for regulating proliferation and differentiation of OPCs into myelinating oligodendrocytes (OLs). However, it remains to be determined whether DNA methylation is also critical for the differentiation of adult OPCs during remyelination. After lysolecithin-induced demyelination in the ventrolateral spinal cord white matter of adult mice of either sex, we detected increased levels of DNA methylation and higher expression levels of the DNA methyltransferase DNMT3A and lower levels of DNMT1 in differentiating adult OLs. To functionally assess the role of DNMT1 and DNMT3 in adult OPCs, we used mice with inducible and lineage-specific ablation of and/or (i.e., , ). Upon lysolecithin injection in the spinal cord of these transgenic mice, we detected defective OPC differentiation and inefficient remyelination in the null and null mice, but not in the null mice. Taken together with previous results in the developing spinal cord, these data suggest an age-dependent role of distinct DNA methyltransferases in the oligodendrocyte lineage, with a dominant role for DNMT1 in neonatal OPCs and for DNMT3A in adult OPCs.
[Mh] Termos MeSH primário: DNA (Citosina-5-)-Metiltransferase 1/metabolismo
DNA (Citosina-5-)-Metiltransferases/metabolismo
Metilação de DNA
Células Precursoras de Oligodendrócitos/metabolismo
Remielinização
Medula Espinal/metabolismo
[Mh] Termos MeSH secundário: Animais
DNA (Citosina-5-)-Metiltransferase 1/genética
DNA (Citosina-5-)-Metiltransferases/genética
Doenças Desmielinizantes/induzido quimicamente
Doenças Desmielinizantes/metabolismo
Feminino
Lisofosfatidilcolinas/administração & dosagem
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Células Precursoras de Oligodendrócitos/ultraestrutura
Substância Branca/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 (Lysophosphatidylcholines); EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferase 1); EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferases); EC 2.1.1.37 (DNA methyltransferase 3A); EC 2.1.1.37 (Dnmt1 protein, mouse)
[Em] Mês de entrada:1801
[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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