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Hippocampal changes in the transcriptome of alpha-synuclein overexpressing mice housed in standard or chronic mild stress environment

ABSTRACT: Hippocampal changes in the transcriptome of alpha-synuclein overexpressing mice housed in standard or chronic mild stress environment

PROVIDER: PRJNA476790 | ENA |

REPOSITORIES: ENA

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Hippocampal changes in the transcriptome of alpha-synuclein overexpressing mice housed in standard or chronic mild stress environment

Project description:Using a mouse model overexpressing human SNCA and profiling the striatal transcriptome, we assessed gene-environment interactions to reveal perturbations in gene expression and their modulation through chronic unpredictable mild stress (CUMS) exposure.

2018-12-13 | GSE116009 | GEO

Distinct Impacts of Alpha-Synuclein Overexpression on the Hippocampal Epigenome of Mice in Standard and Enriched Environments

Project description:Elevated alpha-synuclein (SNCA) gene expression is associated with transcriptional deregulation and increased risk of Parkinson’s disease, which may be partially ameliorated by environmental enrichment. At the molecular level, emerging evidence indicates that excess alpha-synuclein protein (aSyn) impacts the epigenome through direct and/or indirect mechanisms. However, the extents to which both aSyn and the environment converge at the epigenome and whether epigenetic alterations underpin the preventive effects of environmental factors on transcription remain to be elucidated. Here, we profiled five DNA and histone modifications in the hippocampus of wild-type and transgenic mice overexpressing human SNCA. Mice of each genotype were housed under either standard conditions or in an enriched environment (EE) for 12 months. SNCA overexpression induced similar hippocampal DNA hydroxymethylation and H3K27 acetylation changes in both environments, and was associated with environment-dependent changes to H3K4 methylation. These H3K4 methylation changes included loci where the EE ameliorated the impacts of the transgene as well as loci resistant to the effects of environmental enrichment in transgenic mice. In addition, select H3K4 monomethylation alterations were associated with changes in mRNA expression. Our results suggested an environment-dependent impact of excess aSyn on some functionally relevant parts of the epigenome, and will ultimately enhance our understanding of the molecular etiology of Parkinson’s disease and other synucleinopathies.

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Transcriptome and proteome analysis in LUHMES cells overexpressing alpha-synuclein

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The responses of astrocytes stimulated by extracellular a-synuclein

Project description:Abnormal neuronal aggregation of a-synuclein is implicated in the development of Parkinson’s disease. Glial cells also show extensive a-synuclein pathology and are thought to contribute to disease progression. However, the mechanism that produces the glial a-synuclein pathology and the interaction between neurons and glia in the disease-inflicted microenvironment remain unknown. Here, we show that in neuronal cells misfolded a-synuclein proteins are selectively translocated into vesicles, leading to exocytosis of the aggregated forms. More importantly, our data demonstrate that astrocytes take up the neuron-derived a-synuclein aggregates and produce a-synuclein inclusions similar to the ones found in human brains. This uptake is paralleled by changes in the gene expression profile reflecting an inflammatory response. These results suggest that astroglial a-synuclein pathology is produced by cell-to-cell transmission of neuronal a-synuclein aggregates. This transmission step is thus an important mediator of pathogenic glial responses and could qualify as a new therapeutic target. To determine how astrocytes respond to extracellular a-synuclein, gene expression profiles were established and analyzed for nearly 22,000 rat genes using the Illumina RatRef-12 Expression BeadChip. Total RNA was isolated from astrocytes exposed for 6h or 24h to conditioned medium from cultures of a-synuclein or lacZ expressing cells.

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The responses of astrocytes stimulated by extracellular a-synuclein

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Project description: Not available

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