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Transcriptome and proteome analysis in LUHMES cells overexpressing alpha-synuclein

ABSTRACT: Transcriptome and proteome analysis in LUHMES cells overexpressing alpha-synuclein

PROVIDER: PRJNA790940 | ENA |

REPOSITORIES: ENA

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Transcriptome and proteome analysis in LUHMES cells overexpressing alpha-synuclein

Project description:Differential transcriptome analysis in LUHMES cells overexpressing human wild-type alpha-synuclein or GFP

2022-03-31 | GSE191302 | GEO

Transcriptome and proteome analysis in LUHMES cells overexpressing alpha-synculein

Project description:LUHMES cells share many characteritics with human dopamingeric neurons in the substantia nigra, the cells whose demise is responsible for the motor symptoms in Parkinson’s disease (PD). LUHMES cells can therefore be used bona fide as a model to study pathophysiological processes involved in PD. Previously, we showed that LUHMES cell degenerate after six days upon overexpression of wild type alpha-synuclein. In the present study we performed a transcriptome and proteome expression analysis in alpha-synuclein-overexpressing cells and GFP-expressing control cells in order to identify genes and proteins that are differentially regulated upon overexpression of alpha-synuclein. The analysis was performed four days after the initiation of alpha-synuclein or GFP overexpression, before the cells died in order to identify processes that preceded cell death.

2022-05-19 | PXD028322 | Pride

Transcriptome and Proteome Analysis in LUHMES Cells Overexpressing Alpha-Synuclein.

Project description: Not available

| S-EPMC9037753 | biostudies-literature

Alpha-synuclein overexpression is associated with epigenomic dysregulation of glutamate signaling and locomotor pathways

Project description:Although Parkinson’s disease (PD) is one of the most rapidly growing neurological disorders, interindividual differences in PD etiology related to genetics are not fully understood. Here, we demonstrate genome-wide DNA methylation and hydroxymethylation alterations associated with overexpression of two PD-linked alpha-synuclein variants (wild type and A30P) in LUHMES cells differentiated to dopaminergic neurons. Alpha-synuclein altered DNA methylation at thousands of CpGs and DNA hydroxymethylation at hundreds of CpGs in both genotypes, and primarily at locomotor and glutamate signaling pathway genes. In some cases, epigenetic changes were associated with transcription. SMITE network analysis incorporating H3K4me1 ChIP-seq to score DNA methylation and hydroxymethylation changes across promoters, enhancers, and gene bodies confirmed epigenetic and transcriptional deregulation of glutamate signaling modules in both genotypes. Our results identify distinct and shared impacts of alpha-synuclein variants on the epigenome, and associate alpha-synuclein in the epigenetic etiology of PD.

2021-08-02 | GSE181126 | GEO

Single-nuclei transcriptome of enteric neurons in α-synuclein overexpressing mice

Project description:Single-nuclei transcriptome of enteric neurons in α-synuclein overexpressing mice

| PRJNA1262491 | ENA

Systematic characterization of LUHMES cell-based Parkinson’s disease models reveals potential novel drug targets.

Project description:Parkinson's disease (PD) encompasses incurable and progressive loss of dopaminergic neurons in patients and the research for effective disease-modifying treatments are still ongoing. In this study, using a systems biology-based approach we show that 6-OHDA treatment of alpha-synuclein-overexpressing LUHMES cells can be used as a physiologically relevant model of PD. RNAseq analysis in these LUHMES-based disease models validate genes including HMOX1 and IGF2R in common with previously identified PD genes. We further confirm that quercetin and rutin can partially alleviate cell death in this model and show that the expression of genes related to PD as well as those related to mitochondria and energy metabolism are back to basal levels in control cells upon quercetin or rutin pre-treatment. When RNAseq analysis was performed on drug-pretreated LUHMES PD models, protein folding, misfolded protein binding and unfolded protein response pathways were found to be affected. We believe these findings offer new avenues of innovative therapeutic strategies for PD.

2026-01-01 | GSE287941 | GEO

Distinct stress response and altered striatal transcriptome in alpha-synuclein overexpressing mice

Project description:Distinct stress response and altered striatal transcriptome in alpha-synuclein overexpressing mice

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Transcription profiling of transgenic mice overexpressing human alpha-synuclein under the PDGF beta promoter to wildtype littermates at 3 months and 9 months of age.

Project description:Microarray comparison of transgenic mice overexpressing human alpha-synuclein under the PDGF beta promoter to wildtype littermates at 3 months and 9 months of age. RNA was extracted from substantia nigral cells that were isolated by laser capture microdissection.

2007-12-20 | E-MEXP-1383 | biostudies-arrayexpress

Single-nuclei transcriptome of enteric neurons in α-synuclein overexpressing mice

Project description:Overexpression of the neuronal protein α-synuclein (αSyn) is a risk factor for Parkinson’s disease (PD), and αSyn aggregation promotes neurodegeneration and movement disorders. αSyn overexpressing mice (Thy1-ASO) reproduce many PD-associated phenotypes such as motor deficits and constipation, which impacts a majority of patients. We sought to gain insight into enteric nervous system function in Thy1-ASO mice by isolating neuronal nuclei from mouse intestines, which makes up less than 1% of cells, followed by transcriptomic analysis. To overcome the challenge of profiling gene expression in rare cell populations within complex tissues, we engineered an adeno-associated virus (AAV) that expresses a fluorescent protein in the nuclear membrane under the control of a constitutive neuronal promoter. We generated a high-quality single-nuclei gene expression dataset that revealed transcriptional heterogeneity reflecting populations of 4 putative excitatory motor neuron subtypes, 2 putative inhibitory motor neuron subtypes, 3 putative interneuron subtypes, and a putative sensory neuron gene cluster. There was little difference in expression of individual genes in neurons between wild-type and Thy1-ASO mice in the colon, under the conditions tested. However, pathway analysis revealed changes in the PI3K pathway in excitatory motor neurons (upregulated in Thy1-ASO), MAPK and androgen pathways in inhibitory motor neurons (upregulated in Thy1-ASO), and WNT (upregulated in Thy1-ASO) and p53 (downregulated in Thy1-ASO) pathways in interneurons. This dataset can be leveraged to understand the physiological basis of gut motility deficits in α-synuclein overexpressing mice.

2026-06-30 | GSE297092 | GEO

AVE0991 regulates HOTAIRM1/miR-223-3p/α-synuclein to improve behaviour and protect dopaminergic neurons in human α-syn (A53T) overexpressing mice

Project description:Objective: Parkinson's disease (PD) is part of a common type of neurodegenerative disease. AVE0991, a non-peptide analogue of Ang-(1-7), by which the progression of PD has been discovered to be ameliorated, but the specific mechanism whereby AVE0991 modulates the progression of PD remains unclear. Materials and Methods: During the study, the mice overexpressing of human α-syn(A53T) were established to simulate PD pathology, and we also constructed an in vitro model of mouse dopaminergic neurons overexpressing hα-syn(A53T). The [18F] FDG-PET/CT method was also employed to assess FDG uptake in human α-syn(A53T) overexpressing mice. Level of Lnc HOTAIRM1, miR-223-3p were detected via RT-qPCR. Flow cytometry was deployed to assay cell apoptosis. Results: AVE0991 improved behavior disorder and decreased α-syn expression in the substantia nigra in mice with Parkinson's disease. AVE0991 inhibited apoptosis of dopaminergic neurons overexpressing hα-syn(A53T) by LncRNA HOTAIRM1. MiR-223-3p binds to HOTAIRM1 as a ceRNA and directly targets α-syn. Conclusion: The angiotensin-(1–7) analogue AVE0991 targeted the HOTAIRM1/miR-223-3p axis to degrade α-synuclein in PD mice, and showed neuroprotection in vitro.

2024-11-06 | GSE244050 | GEO

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