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Exosome-derived long non-coding RNAs (lncRNAs) are extensively engaged in recovery and repair of the injured spinal cord, through different mechanisms. However, to date no study has systematically evaluated the differentially expressed lncRNAs involved in the development of spinal cord injury. Thus, the aim of this study was to identify key circulating exosome-derived lncRNAs in a rat model of spinal cord injury and investigate their potential actions. To this end, we established a rat model of spinal cord hemisection. Circulating exosomes were extracted from blood samples from spinal cord injury and control (sham) rats and further identified through Western blotting and electron microscopy. RNA was isolated from the exosomes and sequenced. The enrichment analysis demonstrated that there were distinctively different lncRNA and mRNA expression patterns between the two groups. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and Gene Ontology (GO) functional analysis were performed to determine the possible involvements of upregulated and downregulated lncRNAs in various pathways and different biological processes, as well as their cellular locations and molecular functions. Furthermore, quantitative reverse transcription-polymerase chain reaction showed that the expression of five lncRNAs--ENSRN0T00000067908, XR_590093, XR_591455, XR_360081, and XR_346933--was increased, whereas the expression of XR_351404, XR_591426, XR_353833, XR_590076, and XR_590719 was decreased. Of note, these 10 lncRNAs were at the center of the lncRNA-miRNA-mRNA coexpression network, which also included 198 mRNAs and 41 miRNAs. Taken together, our findings show that several circulating exosomal lncRNAs are differentially expressed after spinal cord injury, suggesting that they may be involved in spinal cord injury pathology and pathogenesis. These lncRNAs could potentially serve as targets for the clinical diagnosis and treatment of spinal cord injury.
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http://dx.doi.org/10.4103/1673-5374.353504 | DOI Listing |
Neurol Neuroimmunol Neuroinflamm
November 2025
Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Background And Objectives: Myelitis is a relatively common clinical entity for neurologists, with diverse underlying causes. The aim of this study was to describe the incidence of myelitis, its causes, clinical presentation, and factors predicting functional outcomes and relapses.
Methods: Using the Swedish National Patient Registry, we identified all adult patients in Stockholm County between 2008 and 2018 using International Classification of Diseases, 10th Edition (ICD-10) codes likely to include myelitis.
J Spinal Cord Med
September 2025
Department of Surgery, Hôpital du Sacré-Coeur de Montréal, Montréal, Québec, Canada.
Study Design: A retrospective study with a crossover design.
Objectives: Maintaining mean arterial pressure (MAP) is crucial in the early management of SCI, yet the role of oral midodrine in this setting remains unclear. This study evaluates whether midodrine facilitates IV vasopressor weaning within 24 hours of initiation.
Sci Prog
September 2025
Department of Neurology, University of Afyonkarahisar Health Sciences, Afyonkarahisar, Türkiye.
A considerable number of individuals are diagnosed with idiopathic trigeminal neuralgia. In order to achieve a more complete understanding of the pathophysiology, it is essential to adopt a range of novel approaches and utilize new animal models. This study investigated changes in the messenger RNA (mRNA) expression of ion-channels in a newly developed animal model of trigeminal neuropathic pain induced by cervical spinal dorsal horn compression.
View Article and Find Full Text PDFEur 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.
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