Please use this identifier to cite or link to this item: https://repositorio.ufrn.br/handle/123456789/26100
Full metadata record
DC FieldValueLanguage
dc.contributor.authorGuimarães, Roberta Pereira de Melo-
dc.contributor.authorLandeira, Bruna Soares-
dc.contributor.authorCoelho, Diego Marques-
dc.contributor.authorGolbert, Daiane Cristina Ferreira-
dc.contributor.authorSilveira, Mariana S.-
dc.contributor.authorLinden, Rafael-
dc.contributor.authorReis, Ricardo A. de Melo-
dc.contributor.authorCosta, Marcos Romualdo-
dc.date.accessioned2018-11-12T12:54:25Z-
dc.date.available2018-11-12T12:54:25Z-
dc.date.issued2018-11-12-
dc.identifier.citationGUIMARÃES, R. P. M. et al. Evidence of müller glia conversion into retina ganglion cells using neurogenin2. Frontiers in Cellular Neuroscience, v. 12, n. 410, nov./2018. Disponível em: <https://www.frontiersin.org/article/10.3389/fncel.2018.00410>.pt_BR
dc.identifier.urihttps://repositorio.ufrn.br/jspui/handle/123456789/26100-
dc.languageengpt_BR
dc.rightsAcesso Abertopt_BR
dc.subjectretinapt_BR
dc.subjectmüller glia cellspt_BR
dc.subjectinduced neuronspt_BR
dc.subjectlineage-reprogrammingpt_BR
dc.subjectneurogenin2pt_BR
dc.subjectAscl1pt_BR
dc.subjectretina ganglion cellspt_BR
dc.titleEvidence of müller glia conversion into retina ganglion cells using neurogenin2pt_BR
dc.typearticlept_BR
dc.identifier.doi10.3389/fncel.2018.00410-
dc.description.resumoDegenerative retinopathies are the leading causes of irreversible visual impairment in the elderly, affecting hundreds of millions of patients. Müller glia cells (MGC), the main type of glia found in the vertebrate retina, can resume proliferation in the rodent adult injured retina but contribute weakly to tissue repair when compared to zebrafish retina. However, postnatal and adult mouse MGC can be genetically reprogrammed through the expression of the transcription factor (TF) Achaete-scute homolog 1 (ASCL1) into induced neurons (iNs), displaying key hallmarks of photoreceptors, bipolar and amacrine cells, which may contribute to regenerate the damaged retina. Here, we show that the TF neurogenin 2 (NEUROG2) is also sufficient to lineage-reprogram postnatal mouse MGC into iNs. The efficiency of MGC lineage conversion by NEUROG2 is similar to that observed after expression of ASCL1 and both TFs induce the generation of functionally active iNs. Treatment of MGC cultures with EGF and FGF2 prior to Neurog2 or Ascl1 expression enhances reprogramming efficiencies, what can be at least partially explained by an increase in the frequency of MGCs expressing sex determining region Y (SRY)-box 2 (SOX2). Transduction of either Neurog2 or Ascl1 led to the upregulation of key retina neuronal genes in MGC-derived iNs, but only NEUROG2 induced a consistent increase in the expression of putative retinal ganglion cell (RGC) genes. Moreover, in vivo electroporation of Neurog2 in late progenitors from the neonatal rat retina, which are transcriptionally similar to MGCs, also induced a shift in the generation of retinal cell subtypes, favoring neuronal differentiation at the expense of MGCs and resuming the generation of RGCs. Altogether, our data indicate that NEUROG2 induces lineage conversion of postnatal rodent MGCs into RGC-like iNs in vitro and resumes the generation of this neuronal type from late progenitors of the retina in vivo.pt_BR
Appears in Collections:ICe - Artigos publicados em periódicos

Files in This Item:
File Description SizeFormat 
MarcosCosta_ICe_2018_Evidence of müller.pdfMarcosCosta_ICe_2018_Evidence of müller4,99 MBAdobe PDFThumbnail
View/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.