Dataset Information

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

ABSTRACT: 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.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE296042 | GEO | 2025/05/19

REPOSITORIES: GEO

ACCESS DATA

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Project description:Background: Following spinal cord injury (SCI), the inflammatory storm initiated by microglia/macrophages poses a significant impediment to the recovery process. Exosomes play a crucial role in the transport of miRNAs, facilitating essential cellular communication through the transfer of genetic material. However, the miRNAs from iPSC-NSCs-Exos and their potential mechanisms leading to repair after SCI remain unclear. This study aims to explore the role of iPSC-NSCs-Exos in microglia/macrophage pyroptosis and reveal their potential mechanisms. Methods: iPSC-NSCs-Exos were characterized and identified using transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and Western blot. A mouse SCI model and a series of in vivo and in vitro experiments were conducted to investigate the therapeutic effects of iPSC-NSCs-Exos. Subsequently, miRNA microarray analysis and rescue experiments were performed to confirm the role of miRNAs in iPSC-NSCs-Exos in SCI. Mechanistic studies were carried out using Western blot, luciferase activity assays, and RNA-ChIP. Results: Our findings revealed that iPSC-NSCs-derived exosomes inhibited microglia/macrophage pyroptosis at 7 days post-SCI, maintaining myelin integrity and promoting axonal growth, ultimately improving mice motor function. The miRNA microarray showed let-7b-5p to be highly enriched in iPSC-NSCs-Exos, and LRIG3 was identified as the target gene of let-7b-5p. Through a series of rescue experiments, we uncovered the connection between iPSC-NSCs and microglia/macrophages, revealing a novel target for treating SCI. Conclusion: In conclusion, we discovered that iPSC-NSCs-derived exosomes can package and deliver let-7b-5p, regulating the expression of LRIG3 to ameliorate microglia/macrophage pyroptosis and enhance motor function in mice after SCI. This highlights the potential of combined therapy with iPSC-NSCs-Exos and let-7b-5p in promoting functional recovery and limiting inflammation following SCI.

Dataset Information

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

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets