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Experimental Strategies to Bridge Large Tissue Gaps in the Injured Spinal Cord after Acute and Chronic Lesion
Published on: April 5, 2016
mRNA Profiling for miR-124-mediated Repair in Spinal Cord Injury
Jing Wang1, Haotian Li2, Lingqiang Chen2
1Department of Rheumatology, the First People's Hospital of Yunnan Province, the Affiliated Hospital of Kunming University of Science and Technology, Kunming 650032, Yunnan, China.
Abstract:
The miRNA miR-124 has been reported to be a promising target for the repair of spinal cord injury (SCI), which is a devastating neurological condition. This study aimed to investigate the underlying molecular mechanisms of miR-124-mediated SCI repair. We established miR-124 SCI model rats and further treated them with agomiR-124 for 14 days. After that, their spinal cords were sectioned, and levels of NeuN, GFAP, and NF-200 were measured via immunofluorescence or via immunohistochemistry. In addition, the spinal dorsal horns were collected for sequencing of total RNA. Differentially expressed (DE) mRNAs were then profiled and a number of these were further verified with qPCR. Gene ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed to predict the potential functions of the DE mRNAs. AgomiR-124 was found to significantly inhibit the decrease of neurons and the activation of astrocytes, while promoting NF-200 expression in the dorsal horn. At fourteen days after agomiR-124 treatment, a total of 85 mRNAs were upregulated and 80 mRNAs were downregulated. We focused our analysis of the DE mRNAs on the top 20 most DE mRNAs, and found four upregulated genes (Nploc4, Yme1l1, LOC103693564, and Aspa) and four downregulated genes (Epb41l2, LOC100911685, LOC100910833, and Smarcc1), which are likely to be of interest to SCI researchers. In addition, we noted that Tal1 is a potential target gene of miR-124, and that a low level of this gene promoted the proliferation of neuronal precursor cells and inhibited their differentiation. In conclusion, miR-124 was able to mediate SCI repair by altering the expression of various mRNAs in rats. The miR-124/Tal1 axis may participate in the treatment of SCI by agomiR-124 by repopulating neural stem cells.
Insights
MicroRNA miR-124 promotes spinal cord injury (SCI) repair by modulating gene expression. Treatment with agomiR-124 enhances neuronal survival and promotes neural stem cell repopulation via the miR-124/Tal1 axis.
Area of Science:
- Neuroscience
- Molecular Biology
- Regenerative Medicine
Background:
- Spinal cord injury (SCI) is a debilitating condition with limited treatment options.
- MicroRNA miR-124 has emerged as a potential therapeutic target for SCI repair.
Purpose of the Study:
- To elucidate the molecular mechanisms underlying miR-124-mediated SCI repair.
- To investigate the effects of agomiR-124 treatment on neuronal and glial cells in an SCI model.
Main Methods:
- Established a miR-124 SCI rat model and treated with agomiR-124.
- Assessed neuronal survival (NeuN), astrocyte activation (GFAP), and neurofilament expression (NF-200) via immunofluorescence/immunohistochemistry.
- Performed RNA sequencing and qPCR to identify differentially expressed mRNAs.
- Conducted Gene Ontology and KEGG pathway analyses.
- Investigated the role of the miR-124/Tal1 axis.
Main Results:
- AgomiR-124 treatment significantly reduced neuronal loss and astrocyte activation while increasing NF-200 expression.
- RNA sequencing identified 85 upregulated and 80 downregulated mRNAs.
- Key differentially expressed genes including Nploc4, Yme1l1, Aspa, Epb41l2, and Smarcc1 were identified.
- Tal1 was identified as a potential miR-124 target gene, where low Tal1 levels promoted neuronal precursor cell proliferation.
Conclusions:
- miR-124 plays a crucial role in mediating SCI repair through modulation of mRNA expression.
- The miR-124/Tal1 axis is implicated in SCI treatment by promoting neural stem cell repopulation.
