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Electromagnetic field-mediated direct lineage reprogramming into induced dopamine neurons in vivo for Parkinson's disease therapy

ABSTRACT: Electromagnetic field-mediated direct lineage reprogramming into induced dopamine neurons in vivo for Parkinson's disease therapy

PROVIDER: PRJNA340132 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4064270_1.fastq.gz	Fastqsanger.gz
	SRR4064270_2.fastq.gz	Fastqsanger.gz
	SRR4064269_1.fastq.gz	Fastqsanger.gz
	SRR4064269_2.fastq.gz	Fastqsanger.gz

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Electromagnetic field-mediated direct lineage reprogramming into induced dopamine neurons in vivo for Parkinson’s disease therapy [microarray2]

Project description:Electromagnetic fields (EMF) are physical energy generated by electrically charged objects that can influence numerous biologic processes, including control of cell fate and plasticity. In this study, we show that magnetic gold nanoparticles in the presence of EMF can facilitate efficient direct lineage reprogramming to induced dopamine neurons both in vitro and in vivo. Remarkably, electromagnetic stimulation leads to the specific activation of the histone acetyl transferase Brd2, resulting in H3K27 acetylation and robust activation of neuronal-specific gene expression. In vivo reprogramming in conjunction with EMF stimulation efficiently alleviated symptoms in a mouse model of Parkinson’s disease (PD) in a noninvasive and controllable manner. These studies provide a proof of principle that EMF-based approaches may represent a viable and safe therapeutic strategy facilitating in vivo lineage conversion for neurodegenerative disorders.

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Electromagnetic field-mediated direct lineage reprogramming into induced dopamine neurons in vivo for Parkinson’s disease therapy [microarray1]

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Electromagnetic field-mediated direct lineage reprogramming into induced dopamine neurons in vivo for Parkinson’s disease therapy [ChIP-Seq]

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Mitochondrial proteomics investigation of a cellular model of impaired dopamine homeostasis, an early step in Parkinson's disease pathogenesis

Project description:Impaired dopamine homeostasis is an early event in the pathogenesis of Parkinson's disease. Generation of intracellular reactive oxygen species consequent to dopamine oxidation leads to mitochondrial dysfunction and eventually cell death. Alterations in the mitochondrial proteome due to dopamine exposure were investigated in the SH-SY5Y human neuroblastoma cell line. The combination of two orthogonal proteomic approaches, two-dimensional electrophoresis and shotgun proteomics, was used to highlight the specific pathways perturbed by the increase of intracellular dopamine, in comparison with those perturbed by a specific mitochondrial toxin (4-methyphenylpyridinium, MPP+), a neurotoxin causing Parkinsonism-like symptoms in animal models. Proteins altered by MPP+ did not completely overlap with those affected by dopamine treatment. In particular, the MPP+ target complex I component NADH dehydrogenase [ubiquinone] iron-sulfur protein 3 was not affected by dopamine together with 26 other proteins. The comparison of proteomics approaches highlighted the fragmentation of some mitochondrial proteins, suggesting an alteration of the mitochondrial protease activity. Pathway and disease association analysis of the proteins affected by dopamine revealed the overrepresentation of the Parkinson's disease and the parkin-ubiquitin proteasomal system pathways and of gene ontologies associated to generation of precursor metabolites and energy, response to topologically incorrect proteins and programmed cell death. These alterations may be globally interpreted in part as the result of a direct effect of dopamine on mitochondria (e.g. alteration of the mitochondrial protease activity) and in part as the effect on mitochondria of a general activation of cellular processes (e.g. regulation of programmed cell death).

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Electromagnetic field-mediated direct lineage reprogramming into induced dopamine neurons in vivo for Parkinson's disease therapy

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