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Transcranial direct current stimulation promotes post-SCI motor recovery via miR-298-5p/ LC3-dependent autophagy activation

ABSTRACT: Transcranial direct current stimulation promotes post-SCI motor recovery via miR-298-5p/ LC3-dependent autophagy activation

PROVIDER: PRJNA1257382 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33388292.fastq.gz	Fastqsanger.gz
	SRR33388293.fastq.gz	Fastqsanger.gz
	SRR33388294.fastq.gz	Fastqsanger.gz
	SRR33388295.fastq.gz	Fastqsanger.gz
	SRR33388296.fastq.gz	Fastqsanger.gz

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Transcranial direct current stimulation promotes post-SCI motor recovery via miR-298-5p/ LC3-dependent autophagy activation

Project description:While transcranial direct current stimulation (tDCS) has been shown to contribute to motor recovery after spinal cord injury (SCI), the mechanisms remain unclear. This study investigated whether tDCS exerts neuroprotective effects by regulating apoptosis and autophagy. To achieve this aim, SCI was induced in rats using a modified Allen’s method with tDCS treatment. Otherwise,Furthermore, tDCS-responsive miRNAs were detected by using microRNA (miRNA) sequencing and validated via RT-qPCR. Similarly, tDCS regulatory mechanisms were verified through dual-luciferase assays and miRNA overexpression. Subsequently, H₂O₂-treated PC-12 cells simulated SCI in vitro to examine miR-298-5p's effects on apoptosis and autophagy. The findings revealed that miR-298-5p was upregulated post-SCI and downregulated after tDCS. In vitro, miR-298-5p silencing promoted autophagy and reduced apoptosis, whereas overexpression exacerbated neuronal injury. LC3 was a direct of miR-298-5p, and tDCS enhanced autophagy, reduced apoptosis, improved nerve regeneration, and minimized motor deficits after SCI. Notably, all tDCS-induced effects were counteracted after the overexpression of miR-298-5p by agomir. In summary, this study showed that while miR-298-5p could be detrimental to SCI, tDCS could increase autophagy flux and inhibit neuronal apoptosis by negatively regulating miR-298-5p, thereby improving the recovery of function in SCI.

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Transcranial current stimulation in the sensorimotor cortex of rats alters the expression of immune-mediating genes

Project description:Transcranial direct current stimulation (tDCS) has been applied in experimental and clinical settings for more than twenty years and may facilitate rehabilitation after stroke as suggested by clinical data (Hummel et al. 2005, Sparing et al. 2009). Intriguingly, tDCS evokes various cellular effects exceeding its primary neurophysiological actions: We previously described subacute effects of tDCS on immune- and stem cells in the rat brain (Rueger et al. 2012, Keuters et al. 2015, Pikhovych et al. 2016, Braun et al. 2016). However, the effects of tDCS on immune-mediating genes have not yet been investigated. To investigate the more immediate effects of tDCS regulating those cellular responses, we treated rats with a single session of either anodal or cathodal tDCS, and analyzed the gene expression by microarray; sham-stimulated rats served as control. We confirmed the effects of gene upregulation by immunohistochemistry at the protein level. We here report for the first time that acute anodal transcranial direct current stimulation enhanced the expression of several genes coding for MHC-I, affecting inflammation and synaptic plasticity (Neumann et al. 1995, Shatz et al. 2009). Moreover, cathodal tDCS increased expression of the gene encoding for the immunoregulatory protein Osteopontin. Osteopontin has beneficial effects on neural stem cells and microglia after brain damage such as stroke (Rabenstein et al. 2015, Rabenstein et al. 2016, Ladwig et al. 2017, Rogall et al. 2017). Overall, our data indicate that a specific modulation of neuroinflammatory processes by non-invasive brain stimulation constitutes a promising therapeutic option with immediate translational relevance.

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