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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE163754 | GEO | 2020/12/24

REPOSITORIES: GEO

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

Project description:In order to identify the mRNAs in adult light damaged Muller glia of the the neural retina, Müller glia from Hes-5 GFP reporter mice that were crossed with Swiss Webster mice were isolated by means of fluorescent activated cell sorting and analyzed their mRNAs using the Mouse Gene 1.0 ST microarray (Affymetrix). Differentially expressed genes were analyzed and compared to the genes found upregulated in the Dicer-cKO mouse (Wohl at el., 2017). miRNA:mRNA target tools were used to find potential miRNA targets of Muller glia miRNAs.

2020-12-24 | GSE163753 | GEO

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

Project description:In order to identify the miRNAs in adult light damaged Muller glia of the the neural retina, we isolated the Müller glia from Rlbp-CreER: Stopf/f-tdTomato by means of fluorescent activated cell sorting and analyzed their miRNAs using NanoStrings Technologies®. We compared the data to that from and Dicer1-CKO Müller glia and wild type glia Müller glia (GSE103098). We found three miRNAs potentially regulating genes involved in stress response in both data sets.

2020-12-24 | GSE162993 | GEO

A Comparative Analysis of Reactive Muller Glia Gene Expression After Light Damage and microRNA-Depleted Muller Glia-Focus on microRNAs.

Project description:Müller glia (MG) are the predominant glia in the neural retina and become reactive after injury or in disease. microRNAs (miRNAs) are translational repressors that regulate a variety of processes during development and are required for MG function. However, no data is available about the MG miRNAs in reactive gliosis. Therefore, in this study, we aimed to profile miRNAs and mRNAs in reactive MG 7 days after light damage. Light damage was performed for 8 h at 10,000 lux; this leads to rapid neuronal loss and strong MG reactivity. miRNAs were profiled using the Nanostring platform, gene expression analysis was conducted via microarray. We compared the light damage dataset with the dataset of Dicer deleted MG in order to find similarities and differences. We found: (1) The vast majority of MG miRNAs declined in reactive MG 7 days after light damage. (2) Only four miRNAs increased after light damage, which included miR-124. (3) The top 10 genes found upregulated in reactive MG after light damage include Gfap, Serpina3n, Ednrb and Cxcl10. (4) The miRNA decrease in reactive MG 7 days after injury resembles the profile of Dicer-depleted MG after one month. (5) The comparison of both mRNA expression datasets (light damage and Dicer-cKO) showed 1,502 genes were expressed under both conditions, with Maff , Egr2, Gadd45b, and Atf3 as top upregulated candidates. (6) The DIANA-TarBase v.8 miRNA:RNA interaction tool showed that three miRNAs were found to be present in all networks, i.e., after light damage, and in the combined data set; these were miR-125b-5p, let-7b and let-7c. Taken together, results show there is an overlap of gene regulatory events that occur in reactive MG after light damage (direct damage of neurons) and miRNA-depleted MG (Dicer-cKO), two very different paradigms. This suggests that MG miRNAs play an important role in a ubiquitous MG stress response and manipulating these miRNAs could be a first step to attenuate gliosis.

| S-EPMC7891663 | biostudies-literature

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

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

| PRJNA687423 | ENA

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

Project description:A comparative analysis of reactive Müller glia gene expression after light damage and microRNA-depleted Müller glia – focus on microRNAs [NanoString]

| PRJNA687474 | ENA

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

Project description:A comparative analysis of reactive Müller glia gene expression after light damage and microRNA-depleted Müller glia – focus on microRNAs [Affymetrix]

| PRJNA687475 | ENA

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

Formation of Müller glia-derived progenitor cells in retinas depleted of microglia

Project description:Recent studies have demonstrated the complex coordination of pro-inflammatory signaling and reactive microglia/macrophage on the formation Müller glial-derived progenitor cells (MGPCs) intheretinas offish, birds and mice.We generated scRNA-seq libraries to identify transcriptional changes in Müller glia (MG) that result from the depletion of microglia from the chick retina. We found significant changes in different networks of genes in MG in normal and damaged retinas when the microglia are ablated. We identified a failure of MG to upregulate Wnt-ligands, Heparin binding epidermal growth factor (HBEGF), Fibroblast growth factor (FGF), retinoic acid receptors and genes related to Notch-signaling. Inhibition of GSK3β, to simulate Wnt-signaling, failed to rescue the deficit in formation of proliferating MGPCs in damaged retinas missing microglia. By comparison, application of HBEGF or FGF2 completely rescued the formation of proliferating MGPCs in microglia-depleted retinas. Similarly, injection of a small molecule inhibitor to Smad3 or agonist to retinoic acid receptors partially rescued the formation of proliferating MGPCs in microglia-depleted damaged retinas. According to scRNA-seq libraries, patterns of expression of ligands, receptors, signal transducers and/or processing enzymes to cell-signaling via HBEGF, FGF, retinoic acid and TGFβ are rapidly and transiently upregulated by MG after neuronal damage, consistent with important roles for these cell-signaling pathways in regulating the formation of MGPCs. We conclude that quiescent and activated microglia have a significant impact upon the transcriptomic profile of MG. We conclude that signals produced by reactive microglia in damaged retinas stimulate MG to upregulate cell signaling through HBEGF, FGF and retinoic acid, and downregulate signaling through TGFβ/Smad3 to promote the reprogramming on MG into proliferating MGPCs.

2023-09-14 | GSE242796 | GEO

Comparative proteomic analyses of normal human retina, gliotic PVR retina and human Müller glia

Project description:This study has applied proteomic methodologies to compare protein expression profiles of gliotic and normal human retina as well as established human Müller stem cell lines. It is hoped that this investigation may provide insight into mechanisms of gliosis and also aid studies focusing on endogenous regeneration of the retina following disease or injury

2018-09-06 | PXD008485 | Pride

Fullerol rescues the light-induced retinal damage by modulating Muller glia cell fate.

Project description:Excessive light exposure can damage photoreceptors and lead to blindness. Oxidative stress serves a key role in photo-induced retinal damage. Free radical scavengers have been proven to protect against photo-damaged retinal degeneration. Fullerol, a potent antioxidant, has the potential to protect against ultraviolet-B (UVB)-induced cornea injury by activating the endogenous stem cells. However, its effects on cell fate determination of Müller glia (MG) between gliosis and de-differentiation remain unclear. Therefore, we established a MG lineage-tracing mouse model of light-induced retinal damage to examine the therapeutic effects of fullerol. Fullerol exhibited superior protection against light-induced retinal injury compared to glutathione (GSH) and reduced oxidative stress levels, inhibited gliosis by suppressing the TGF-β pathway, and enhanced the de-differentiation of MG cells. RNA sequencing revealed that transcription candidate pathways, including Nrf2 and Wnt10a pathways, were involved in fullerol-induced neuroprotection. Fullerol-mediated transcriptional changes were validated by qPCR, Western blotting, and immunostaining using mouse retinas and human-derived Müller cell lines MIO-M1 cells, confirming that fullerol possibly modulated the Nrf2, Wnt10a, and TGF-β pathways in MG, which suppressed gliosis and promoted the de-differentiation of MG in light-induced retinal degeneration, indicating its potential in treating retinal diseases.

| S-EPMC10570010 | biostudies-literature

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