Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1099939 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28674700_1.fastq.gz | Fastqsanger.gz | |||
| SRR28674700_2.fastq.gz | Fastqsanger.gz | |||
| SRR28674800_1.fastq.gz | Fastqsanger.gz | |||
| SRR28674800_2.fastq.gz | Fastqsanger.gz | |||
| SRR28674701_1.fastq.gz | Fastqsanger.gz |
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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.
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Project description:In order to investigate the effect of Alpha-Ketoglutarate (AKG) on p-α-synuclein in substantia nigra of Parkinson's disease (PD) model mice (C57BL/6), we profiled substantia nigra from wild-type (WT), AAV-α-synuclein (α-Syn), AKG and α-Syn-AKG in male mice by RNA sequencing (RNA-seq).
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Project description:Kuznetsov2016(II) - α-syn aggregation
kinetics in Parkinson's
This theoretical model uses 2-step Finke-Watzky (FW) kinetics
todescribe the production, misfolding, aggregation, transport and
degradation of α-syn that may lead to Parkinson's Disease
(PD). Deregulated α-syn degradation is predicted to be
crucialfor PD pathogenesis.
This model is described in the article:
What can trigger the onset
of Parkinson's disease - A modeling study based on a
compartmental model of α-synuclein transport and aggregation in
neurons.
Kuznetsov IA, Kuznetsov AV.
Math Biosci 2016 Aug; 278: 22-29
Abstract:
The aim of this paper is to develop a minimal model
describing events leading to the onset of Parkinson's disease
(PD). The model accounts for α-synuclein (α-syn) production in
the soma, transport toward the synapse, misfolding, and
aggregation. The production and aggregation of polymeric α-syn
is simulated using a minimalistic 2-step Finke-Watzky model. We
utilized the developed model to analyze what changes in a
healthy neuron are likely to lead to the onset of α-syn
aggregation. We checked the effects of interruption of α-syn
transport toward the synapse, entry of misfolded (infectious)
α-syn into the somatic and synaptic compartments, increasing
the rate of α-syn synthesis in the soma, and failure of α-syn
degradation machinery. Our model suggests that failure of α-syn
degradation machinery is probably the most likely cause for the
onset of α-syn aggregation leading to PD.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000615.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000615 | BioModels
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2024-12-02 | GSE278265 | GEO
Project description:Parkinson's disease is the second most common neurodegenerative disorder, whose characteristic pathology involves progressive loss of dopaminergic neurons and formation of Lewy bodies(LBs) in the substantia nigra(SN). Aggregated and misfolded α-synuclein(α-syn) is the major constituent of LBs. As the newly discovered pathway of renin-angiotensin system (RAS), Angiotensin-(1-7)(Ang-(1-7)) and its receptor Mas have attracted increasing attentions for their correlation with PD progression, but underlying mechanisms remain not very clear. Based on the above, this study established PD models of mice and primary dopaminergic neurons with overexpression of α-syn, then discussed the effect of Ang-(1-7)/Mas on these models combined with downstream lncRNA and miRNA. The findings show that Ang-(1-7) alleviates behavioral disorders, rescues dopaminergic neurons loss and lowers α-syn expression in the SN of hα-syn(A53T) overexpressed PD mice. We also discover that Ang-(1-7) decreases the level of α-syn and apoptosis in the hα-syn(A53T) overexpressed dopaminergic neurons through NEAT1/miR-153-3p axis. Moreover, miR-153-3p expression in peripheral blood is found negatively correlated with that of α-syn. These results not only uncovered the significance and related mechanisms of Ang-(1-7)/Mas on α-syn pathology, but also throwed a new light upon miR-153-3p and NEAT1 as biomarkers and therapeutic targets in PD.
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