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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE86049 | GEO | 2018/04/10

REPOSITORIES: GEO

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Project description:Consistent and independently replicated laboratory evidence to support a causative relationship between environmental exposure to extremely low frequency electromagnetic fields (ELF-EMF) at power line frequencies and the associated increase in risk of childhood leukaemia has not been obtained. In particular, although gene expression responses have been reported in a wide variety of cells, none have emerged as robust, widely replicated effects. DNA microarrays facilitate comprehensive searches for changes in gene expression without a requirement to select candidate responsive genes. To determine if gene expression changes occur in white blood cells of volunteers exposed to an ELF-EMF, each of 17 pairs of male volunteers age 20-30 was subjected either to a 50 Hz EMF exposure of 62.0 ± 7.1 μT for 2 h or to a sham exposure (0.21 ± 0.05 μT) at the same time (11:00-13:00). The alternative regime for each volunteer was repeated on the following day and the two-day sequence was repeated 6 days later except that a null exposure (0.085 ± 0.01 μT) replaced the sham exposure. Five blood samples (10 ml) were collected at 2 h intervals from 9:00 to 17:00 with five additional samples during the exposure and sham or null exposure periods on each study day at 11.05, 11.10, 11.20, 11.40 and 12.20. RNA samples were pooled for the same time points on each study day for the 17 volunteers that were subjected to the ELF-EMF exposure/sham or null exposure sequence and were analysed on Illumina microarrays. Time courses for 16 mammalian genes previously reported to be responsive to ELF-EMF exposure, including immediate early genes, stress response, cell proliferation and apoptotic genes were examined in detail. No genes or gene sets significantly expressed on the arrays showed consistent response profiles to repeated ELF-EMF exposures. A stress response was detected as a transient increase in plasma cortisol at the onset of either exposure or sham exposure on the first study day. The cortisol response diminished progressively on subsequent exposures or sham exposures and was attributable to mild stress associated with the experimental protocol. The study design described in the summary gave a total of 40 pooled RNA samples (10 for each study day) using equal amounts of RNA from the 17 volunteers exposed to ELF-EMF on study days 1 and 3, a sham exposure on study day 2 and a null exposures on study day 4. The pooled sample from 11:00 on Day1 (immediately prior to ELF-EMF exposure) was used as a reference sample that was amplified and labelled 4 times with the other samples from each of the 4 study days (titled as replicates 1 to 4). Each replicate was hybridised twice (titled replicates a and b for each day ( e.g. 1a, 1b) to give a total of 8 arrays from the reference RNA sample (Sample names 2 and 41-47, i.e.GSM879110-GSM879117).

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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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