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MicroRNAs miR-25, let-7 and miR-124 regulate the neurogenic potential of Müller glia in mice

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE135846 | GEO | 2019/08/14

REPOSITORIES: GEO

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MicroRNAs miR-25, let-7 and miR-124 regulate the neurogenic potential of Muller glia in mice.

Project description: Not available

| S-EPMC6765125 | biostudies-literature

MicroRNAs miR-25, let-7 and miR-124 regulate the neurogenic potential of Müller glia in mice [NanoString]

Project description:In order to identify the miRNAs in postnatal day 2 (P2) retinal progenitor cells (RPCs), and P8, P11, and adult Müller glia (MG) of the neural retina, we isolated the retinal progenitors from Sox2-CreER: Stopf/f-tdTomato and MG from Rlbp-CreER: Stopf/f-tdTomato mice by means of fluorescent activated cell sorting and analyzed their miRNAs using NanoStrings Technologies®. We next compared miRNA expression of RPCs with MG. We found that most specific miRNAs decline with glial maturation (RPC miRNAs) while others increase (MG miRNAs). Overexpression of miRNA-25 found in RPCs and inhibition of MG miRNA let-7 can induce a neurogenic potential in MG and initiates a de novo differentiation toward neuronal fates.

2019-08-14 | GSE135835 | GEO

MicroRNAs miR-25, let-7 and miR-124 regulate the neurogenic potential of Müller glia in mice [RNA-Seq]

Project description:Müller glial cells (MG) generate retinal progenitor (RPC)-like cells after injury in non-mammalian species, though this does not occur in the mammalian retina. Studies have profiled gene expression in these cells to define genes that may be relevant to their differences in neurogenic potential. However, less is known about differences in micro-RNA (miRNA) expression. In this study, we compared miRNAs from RPCs and MG to identify miRNAs more highly expressed in RPCs, and others more highly expressed in MG. To determine whether these miRNAs are relevant to the difference in neurogenic potential between these two cell types, we tested them in dissociated cultures of MG using either mimics or antagomiRs to increase or reduce expression, respectively. Among the miRNAs tested, miR-25 and miR-124 over-expression, or let-7 antagonism, induced Ascl1 expression and conversion of approximately 40% of mature MG into a neuronal/RPC phenotype. Our results suggest that the differences in miRNA expression between MG and RPCs contribute to their difference in neurogenic potential and that manipulations in miRNAs provide a new tool to reprogram MG for retinal regeneration.

2019-08-14 | GSE135816 | GEO

MicroRNAs miR-25, let-7 and miR-124 regulate the neurogenic potential of Müller glia in mice

Project description:MicroRNAs miR-25, let-7 and miR-124 regulate the neurogenic potential of Müller glia in mice

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MicroRNAs miR-25, let-7 and miR-124 regulate the neurogenic potential of Müller glia in mice [NanoString]

Project description:MicroRNAs miR-25, let-7 and miR-124 regulate the neurogenic potential of Müller glia in mice [NanoString]

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MicroRNAs miR-25, let-7 and miR-124 regulate the neurogenic potential of Müller glia in mice [RNA-Seq]

Project description:MicroRNAs miR-25, let-7 and miR-124 regulate the neurogenic potential of Müller glia in mice [RNA-Seq]

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MicroRNAs miR-124 and miR-135a are potential regulators of the mineralocorticoid receptor gene (NR3C2) expression.

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miR-124-9-9* potentiates Ascl1-induced reprogramming of cultured Muller glia.

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Expression profiling of Ascl1-reprogrammed P12 Müller glia compared with freshly dissociated progenitors and Müller glia

Project description:Non-mammalian vertebrates have a robust ability to regenerate injured retinal neurons from Müller glia cells (MG) that activate the proneural factor Achaete-scute homolog 1 (Ascl1/Mash1) and de-differentiate into progenitors cells. In contrast, mammalian MG have a limited regenerative response and fail to upregulate Ascl1 after injury. To test whether Ascl1 could restore a neurogenic potential to mammalian MG, we over-expressed Ascl1 in dissociated mouse MG cultures and intact retinal explants. Ascl1-infected MG upregulate retinal progenitor-specific genes, while downregulating glial genes. Furthermore, Ascl1 remodeled the chromatin at its targets from a repressive to active configuration. MG-derived progenitors differentiated into cells that exhibited neuronal morphologies, expressed retinal subtype-specific neuronal markers, and displayed neuron-like physiological responses. These results indicate that a single transcription factor, Ascl1, can produce a neurogenic state in mature Muller glia. Expresssion profiling was used to determine the genes that were changed after Ascl1 infection of P12 cultured Müller glia compared with those present in P0 progenitors and P7-P21 Müller glia Retinas were dissociated and FAC-sorted from Hes5-GFP mice at P0, P7, P10, P14 or P21 and submitted for profiling. WT Retinas were dissociated at P12, grown for 1 week in culture, and infected with lentiviruses expressing Ascl1 or GFP for four days. Total RNA was extracted and submitted for profiling.

2013-04-06 | E-GEOD-45835 | biostudies-arrayexpress

A comparative analysis of reactive Müller glia gene expression after light damage and microRNA-depleted Müller glia – focus on microRNAs

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-12-24 | GSE163754 | GEO