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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of rat perineuronal A2B5/OTMP+ oligodendrocytes

ABSTRACT: Oligodendrocytes are cells from the central nervous system that can be grouped into precursors, myelin-forming, and non-myelinating perineuronal. The function of perineuronal oligodendrocytes is unknown; it was suggested that they can ensheath denuded axons. We tested this hypothesis. Using cell-specific tags, microarray technology and bioinformatics tools to identify gene expression differences between these subpopulations allowed us to capture the genetic signature of perineuronal oligodendrocytes. Here we report that perineuronal oligodendrocytes are configured for a dual role. As perineuronal, they integrate a repertoire of transcripts designed to create a cell with its own physiological agenda. But they maintain a reservoir of untranslated transcripts encoding the major myelin proteins for â we speculate â a pathological eventuality. We posit that the signature molecules PDGFR-Î±Î², cytokine PDGF-CC, and the transcription factor Pea3 used â among others - to define the non-myelinating phenotype, may be critical for mounting a myelinating programme during demyelination. Harnessing this capability is of therapeutic value for diseases such as multiple sclerosis. This is the first molecular characterization of perineuronal oligodendrocytes. Experiment Overall Design: Flow Cytometry was used to isolate A2B5/OTMP+ oligodendrocytes from postnatal day 7 rat brain. 4 bioloical replicates were obtained. This data can be compared to the previously submitted oligodendrocyte expression data (GSE5940).

ORGANISM(S): Rattus norvegicus

SUBMITTER: Joe Nielsen

PROVIDER: E-GEOD-11277 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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A2B5/OTMP+ rat perineuronal oligodendrocytes

Project description:Oligodendrocytes are cells from the central nervous system that can be grouped into precursors, myelin-forming, and non-myelinating perineuronal. The function of perineuronal oligodendrocytes is unknown; it was suggested that they can ensheath denuded axons. We tested this hypothesis. Using cell-specific tags, microarray technology and bioinformatics tools to identify gene expression differences between these subpopulations allowed us to capture the genetic signature of perineuronal oligodendrocytes. Here we report that perineuronal oligodendrocytes are configured for a dual role. As perineuronal, they integrate a repertoire of transcripts designed to create a cell with its own physiological agenda. But they maintain a reservoir of untranslated transcripts encoding the major myelin proteins for – we speculate – a pathological eventuality. We posit that the signature molecules PDGFR-αβ, cytokine PDGF-CC, and the transcription factor Pea3 used – among others - to define the non-myelinating phenotype, may be critical for mounting a myelinating programme during demyelination. Harnessing this capability is of therapeutic value for diseases such as multiple sclerosis. This is the first molecular characterization of perineuronal oligodendrocytes. Keywords: developmental

2008-06-01 | GSE11277 | GEO

Transcription profiling of differentiation of Rattus norvegicus oligodendrocytes from their progenitor cells

Project description:Oligodendrocytes undergo extensive changes as they differentiate from progenitors into myelinating cells. To better understand the; molecular mechanisms underlying this transformation, we performed a comparative analysis using gene expression profiling of A2B5+; oligodendrocyte progenitors and O4+ oligodendrocytes. Cells were sort-purified ex vivo from postnatal rat brain using flow cytometry. Using Affymetrix microarrays, 1707 transcripts were identified with a more than twofold increase in expression inO4+oligodendrocytes. Many genes required for oligodendrocyte differentiation were upregulated in O4+ oligodendrocytes, including numerous genes encoding; myelin proteins. Transcriptional changes included genes required for cell adhesion, actin cytoskeleton regulation, and fatty acid and; cholesterol biosynthesis. At the O4+ stage, there was an increase in expression of a novel proline-rich transmembrane protein (Prmp). Localized to the plasma membrane, Prmp displays adhesive properties that may be important for linking the extracellular matrix to the; actin cytoskeleton. Together, our results highlight the usefulness of this discovery-driven experimental strategy to identify genes relevant; to oligodendrocyte differentiation and myelination. Experiment Overall Design: Whole brain dissociates were prepared from one litter of 10 male postnatal day 7 rat pups for each of the 5 A2B5 bioligcal replicates and the 4 O4+ bioligical replicates. Total RNA was extracted from single A2B5+ and single O4+ cells sorted directly from postnatal day7 rat whole brain dissociates using flow cytometry.

2007-11-29 | E-GEOD-5940 | biostudies-arrayexpress

Gene Expression Profiling of Primary Rat Oligodendrocytes

Project description:Oligodendrocytes undergo extensive changes as they differentiate from progenitors into myelinating cells. To better understand the molecular mechanisms underlying this transformation, we performed a comparative analysis using gene expression profiling of A2B5+ oligodendrocyte progenitors and O4+ oligodendrocytes. Cells were sort-purified ex vivo from postnatal rat brain using flow cytometry. Using Affymetrix microarrays, 1707 transcripts were identified with a more than twofold increase in expression inO4+oligodendrocytes. Many genes required for oligodendrocyte differentiation were upregulated in O4+ oligodendrocytes, including numerous genes encoding myelin proteins. Transcriptional changes included genes required for cell adhesion, actin cytoskeleton regulation, and fatty acid and cholesterol biosynthesis. At the O4+ stage, there was an increase in expression of a novel proline-rich transmembrane protein (Prmp). Localized to the plasma membrane, Prmp displays adhesive properties that may be important for linking the extracellular matrix to the actin cytoskeleton. Together, our results highlight the usefulness of this discovery-driven experimental strategy to identify genes relevant to oligodendrocyte differentiation and myelination. Keywords: develepmental stage, oligodendrocyte differentiation

2006-09-30 | GSE5940 | GEO

Transcription profiling of rat oligodendrocyres to identify dynamically regulated microRNA and mRNA Networks

Project description:MicroRNAs (miRNAs) play important roles in modulating gene expression at the post-transcriptional level. In postnatal oligodendrocytes, the miRNA expression profile -â??microRNAomeâ?? - consists of 98 miRNAs whose expression dynamically changes during the transition from A2B5+ oligodendrocyte progenitor cells to premyelinating GalC+ cells. The combination of microRNAome profiling with analyses of the oligodendrocyte transcriptome reveals a target bias for a class of miRNAs which includes miR-9. We show that miR-9 is down-regulated during oligodendrocyte differentiation. In addition, miR-9 expression levels inversely correlate with the expression of its predicted targets, among which is the peripheral myelin protein, PMP22. PMP22 mRNA but not protein is detectable in oligodendrocytes, while Schwann cells producing PMP22 protein lack miR-9. We demonstrate that miR-9 interacts with the 3â?? untranslated region of PMP22 and down-regulates its expression. Our results support models in which miRNAs can act as guardians of the transcriptome. Experiment Overall Design: Flow cytometry was used to isolate single A2B5+ and single GalC+ oligodedrocytes from postnatal day 7 rat whole brain. 4 biological replicates were obtained for each group using a pooled litter of 10 pups per biological replicate

2008-06-18 | E-GEOD-11218 | biostudies-arrayexpress

Progressive axonopathy when oligodendrocytes lack the myelin protein CMTM5

Project description:Chemokine-like factor-like MARVEL-transmembrane domain containing protein 5 (CMTM5) is a tetraspan-transmembrane protein highly enriched in oligodendrocytes and central nervous system (CNS) myelin. We analyzed the proteome of myelin biochemically purified from mouse brains upon genetic disruption of the Cmtm5-gene specifically in myelinating cells. An ion mobility-enhanced version of data-independent acquisition (DIA) workflow with alternating low and elevated energy (referred to as UDMSE) was used to compare protein abundance in Cmtm5 cKO and CTRL samples by label-free quantification. Specifically, dynamic range enhancement (DRE)-UDMSE was applied as a dedicated data acquisition mode recently introduced for routine differential myelin proteome profiling. We found that Cmtm5 cKO mice displayed a largely similar myelin proteome composition as control mice and, together with other data such as electron micrographs, concluded that CMTM5 is not essential for myelin biogenesis and composition. However, oligodendroglial Cmtm5-deficiency causes an early-onset progressive axonopathy, presumably following a Wallerian-like pathomechanism. These results indicate that CMTM5 is involved in the function of oligodendrocytes to maintain axonal integrity rather than myelin biogenesis.

2022-04-04 | PXD029443 | Pride

Genetically perturbed myelin as a risk factor for neuroinflammation-driven axon degeneration

Project description:Axon degeneration and neurological dysfunction in myelin diseases is often attributed to loss of myelin. Perturbed myelinating glia can instigate chronic neuroinflammation and contribute to demyelination and axonal damage. We have previously shown in mice that distinct defects in the proteolipid protein 1 gene result in axonal damage which is largely driven by cytotoxic T cells targeting myelinating oligodendrocytes. Here we show in these mutants that persistent ensheathment with perturbed myelin poses a risk for axon degeneration, neuron loss, and behavioral decline. We demonstrate that CD8+ T cell-driven axonal damage is less likely to progress towards degeneration when axons are efficiently demyelinated by activated microglia. Mechanistically, we show that cytotoxic T cell effector molecules induce aberrant cytoskeletal plasticity within myelinating glial processes and constriction of axons at paranodal domains. Our study identifies detrimental axon-glia interactions which promote neurodegeneration and possible therapeutic targets for disorders associated with myelin defects and neuroinflammation.

2023-09-29 | GSE224032 | GEO

Rattus norvegicus

Project description:A2B5/OTMP+ rat perineuronal oligodendrocytes

| PRJNA106679 | ENA

Identification of Myelin-gene Regulatory Factor as a Critical Transcriptional Regulator Required for CNS Myelination

Project description:The transcriptional control of CNS myelin gene expression is poorly understood. Here we identify gene model 98, which we have named Myelin-gene Regulatory Factor (MRF), as a transcriptional regulator required for CNS myelination. Within the CNS, MRF is specifically expressed by postmitotic oligodendrocytes. MRF is a nuclear protein containing an evolutionarily conserved DNA binding domain homologous to a yeast transcription factor. Knockdown of MRF in oligodendrocytes by RNA interference prevents expression of most CNS myelin genes; conversely, overexpression of MRF within cultured oligodendrocyte progenitors or the chick spinal cord promotes expression of myelin genes. In mice lacking MRF within the oligodendrocyte lineage, pre-myelinating oligodendrocytes are generated but display severe deficits in myelin gene expression and fail to myelinate. These mice display severe neurological abnormalities, and die due to seizures during the third postnatal week. These findings establish MRF as a critical transcriptional regulator essential for oligodendrocyte maturation and CNS myelination. We used microarrays to compare cultured oligodendrocytes (differentiated in vitro for 4 days) from MRF conditional knockouts and control litteramates to look at the effects of MRF deficiency on myelin gene expression. Mouse OPCs grown in vitro in the presence of PDGF serve as a baseline for gene expression prior to differentiation.

2009-05-31 | GSE15303 | GEO

RNA-seq of myelinating oligodendrocytes in Lmna wt and knockout mice

Project description:We showed that the composition of the nucler lamina changes with the differentiation state of oligodendrocyte lineage cells, with Lamin B highly expressed in progenitor cells and Lamin A highly expressed in mature oligodendrocytes. The genetic deletion of Lmna in oligodendrocytes results in the onset of a progressive motor phenotype in adult mice. We performed RNA-Seq in myelinating oligodendrocytes expressing the reporter myelin marker NDRG1-EGFP ( Marechal et al., 2021) in the presence or absence of LMNA. The goal is to identify the transcriptome profile in mice LMNA ablated cells compared to the controls.

2023-06-21 | GSE222574 | GEO

ChIP-sequencing of STAT3 in Zdhhc5 knockout oligodendrocytes

Project description:Myelin sheath is an important structure to maintain normal functions of the nerves in central nervous system. Protein palmitoylation has been established as a sorting determinant for the transport of myelin-forming proteins to the myelin membrane. However, its function in the regulation of oligodendrocyte development remains unknown. Here, we show that an Asp-His-His-Cys (DHHC) motif-containing palmitoyl acyltransferases, DHHC5, is involved in the control of oligodendrocyte development. Loss of Zdhhc5 in oligodendrocytes inhibits myelination and remyelination by a reduction on total myelinating oligodendrocyte population. STAT3 is the primary substrate for DHHC5 palmitoylation in oligodendrocytes. Zdhhc5 ablation reduces STAT3 palmitoylation, and then suppresses STAT3 phosphorylation and activation. As a result of the decreased STAT3 transactivity, the transcription of the myelin-related and anti-apoptosis genes is therefore inhibited, leading to suppressed oligodendrocyte development and myelination. Our findings demonstrate the key role DHHC5 in the control of myelinogenesis.

2024-02-04 | GSE169248 | GEO

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