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Background: Previous research shows that scar tissue formed in the injured area after spinal cord injury blocks nerve regeneration and functional recovery. However, those researchers tried to prevent the formation of scar after spinal cord injury to promote nerve regeneration, but it ran counter to their desire, indicating that the formation of scar might play a role in functional recovery after spinal cord injury.
Methods: To investigate roles of scar formation on functional repair after spinal cord injury, we selected several different key time points to resect the scar tissue formed after spinal cord injury based on the rat models of the T8-T9 transection injury of spinal cord. First, the recovery of motor function was evaluated by Basso Beattie Bresnahan score and electrophysiologic examination; second, the pathologic features of functional recovery were analyzed mainly by immunofluorescence βⅢ-tubulin staining; finally, the genes related to the recovery of motor function were predicted by high-throughput sequencing analysis.
Results: Immunofluorescence results showed that the resection of scar tissue promoted significantly the recovery of motor function and the expression of βⅢ-tubulin in the injured area in the second week after spinal cord injury. Furthermore, RNA-seq studies showed that Tubb3 and Tubb6 gene expression and other neural regeneration pathways were significantly different in the tissue before and after early resection.
Conclusions: Excision of scar tissue in the second week promoted nerve regeneration after spinal cord injury. Tubb3 and Tubb6 genes might be the potential targets for spinal cord injury therapy in our study.
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http://dx.doi.org/10.1016/j.wneu.2022.10.069 | DOI Listing |
Eur Spine J
September 2025
Consultant Neurosurgeon, Centre for Functional Neurosurgery, University Hospital Southampton NHS Foundation Trust, Southampton, UK.
Stem Cell Rev Rep
September 2025
Stem Cells and Metabolism Research Program (STEMM), Research Programs Unit, Faculty of Medicine, University of Helsinki, Helsinki, 00014, Finland.
Mutations in Delta Like Non-Canonical Notch Ligand 1 (DLK1), a paternally expressed imprinted gene, underlie central precocious puberty (CPP), yet the mechanism remains unclear. To test the hypothesis that DLK1 plays a role in gonadotropin releasing hormone (GnRH) neuron ontogeny, 75 base pairs were deleted in both alleles of DLK1 exon 3 with CRISPR-Cas9 in human pluripotent stem cells (hPSCs). This line, exhibiting More than 80% loss of DLK1 protein, was differentiated into GnRH neurons by dual SMAD inhibition (dSMADi), FGF8 treatment and Notch inhibition, as previously described, however, it did not exhibit accelerated GNRH1 expression.
View Article and Find Full Text PDFPain
August 2025
Centre for Multimodal Sensorimotor and Pain Research, Faculty of Dentistry, University of Toronto, Toronto, ON, Canada.
The thermal grill, in which innocuous warm and cool stimuli are interlaced, can produce a paradoxical burning pain sensation-the thermal grill illusion (TGI). Although the mechanisms underlying TGI remain unclear, prominent theories point to spinal dorsal horn integration of innocuous thermal inputs to elicit pain. It remains unknown whether the TGI activates peripheral nociceptors, or solely thermosensitive afferents that are integrated within the spinal cord to give rise to a painful experience.
View Article and Find Full Text PDFNeurol Res
September 2025
Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
Objectives: This study aimed to investigate the effects of repeated exposure to sevoflurane as an anesthetic agent during various developmental stages, namely neonatal, preadolescent, and adult, on behavioral, synaptic, and neuronal plasticity in male and female Wistar rats.
Methods: Rats were exposed to sevoflurane during three developmental stages: neonatal (PN7), pre-adolescence (PN28), and adulthood (PN90). Behavioral performance was evaluated with the Morris Water Maze.
Neurol Res
September 2025
Henan Provincial People's Hospital, Department of Surgery of Spine and Spinal Cord, People's Hospital of Zhengzhou University, Zhengzhou, China.
Background: Immunotherapy holds significant yet underexplored potential for low-grade glioma (LGG) treatment. We therefore interrogated the role of Fanconi Anemia Complementation Group C (FANCC) as a novel immune checkpoint regulator given its spatial correlation with tumor microenvironments and clinical associations with immunosuppressive markers.
Objectives: FANCC is implicated in various tumor progressions; its role in LGG remains unexplored.