Single-cell RNA sequencing of T cells from the spleen and spinal cord
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE271037 | GEO | 2026/01/13
REPOSITORIES: GEO
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Project description:Spinal cord injury (SCI) induces both intraspinal damage and systemic organ pathology, with aging as a major determinant of outcome. However, how advanced age exacerbates SCI pathology remains unclear. The voltage-gated proton channel Hv1, a regulator of immune activation, increases with age and after SCI, and its deletion is neuroprotective in young mice. Thus, we hypothesized that age-related Hv1 upregulation worsens spinal cord, spleen, and lung pathology and hinders locomotor recovery after SCI through immune modulation. Using aged Hv1 KO and WT male mice subjected to moderate SCI, we assessed behavioral and molecular outcomes. Transcriptomic analysis revealed that Hv1 mRNA expression was higher in the brains of aged sham mice and further upregulated in injured spinal cord tissues. Spinal cord RNA-seq showed acute innate immune and cytokine activation in both genotypes. Hv1 deletion enhanced chromatin remodeling, epigenetic and Wnt signaling, while suppressing NF-κB–driven inflammation and oxidative stress–induced apoptosis. In the spleen, Hv1 depletion enhanced immune responses while suppressing mitosis. T cell and leukocyte activation increased, whereas lung cytokine signaling decreased. At 6 weeks after SCI, Hv1 KO mice showed elevated expression of genes related to circadian rhythm and T cell proliferation in the spinal cord, increased mitotic gene expression but reduced adaptive immunity in the spleen, and enhanced immune activation with decreased cilium activity in the lungs.
2025-12-17 | GSE313209 | GEO
Project description:The aneurysm clip impact-compression model of spinal cord injury (SCI) in animals mimics the primary mechanism of SCI in human, i.e. acute impact and persisting compression; and its histo-pathological and behavioural outcomes are extensively similar to the human SCI. In order to understand the distinct molecular events underlying this injury model, an analysis of global gene expression of the acute, subacute and chronic stages of a moderate to severe injury to the rat spinal cord was conducted using a microarray gene chip approach. Rat thoracic spinal cord (T7) was injured using aneurysm clip impact-compression injury model and the epicenter area of injured spinal cord was isolated for RNA extraction and processing and hybridization on Affymetrix GeneChip arrays.
2013-11-15 | E-GEOD-45006 | biostudies-arrayexpress
Project description:LncRNAs played a crucial role in the cell growth, development and some diseases relating to central nerve system.This study suggest that with regulating the LncRNAs expression level we might design novel therapy for spinalcord injury. In this dataset, we profiled the expression pattern of LncRNAs by microarray method after spinal cord injury (SCI). Through Gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis seek LncRNAs potential function in the repair of spinal cord injury. Fifteen samples were analyzed. In these sample, we divided into five groups (sham operation, 1 day post-injured, 3 days post-injured, 1 week post-injued and 3 weeks post-injured) and each group contained three mice.After RNA extraction,RNA form mice in the same group were mixed by equal mass for the preparation of microarray.Compared with spinal cord without injury, the differential expression level of LncRNAs had a few changes at 1day post-injury, reached the peak at 1 week after SCI, and subsequently declined until 3 weeks post-injury. Genes with an FDR≤0.05 and a fold-change ≥2 were selected. Subsequently we analysis the significant differential expression genes.
2015-09-01 | E-GEOD-67515 | biostudies-arrayexpress
Project description:Spinal cord injury (SCI) refers to the damage to the spinal cord due to trauma, disease or degeneration, and the number of new cases is increasing yearly. The changes of cells in the area of SCI are significant to tissue injury. However, the changes in cellular composition, the trajectory of cell development and the interesting relationship of intercellular communication in the injured area are still unclear. In this study, we used single-cell RNA sequencing to evaluate almost all the cell types that make up the site of SCI in rats.
2024-07-01 | GSE213240 | GEO
Project description:Spinal cord injury (SCI) evokes profound dysfunction in hollow organs such as the urinary bladder and gut. Current treatments are limited by a lack of molecular data to inform novel therapeutic avenues. Previously, we showed systemic treatment with the neuroprotective agent inosine improved bladder function following SCI in rats. This RNA-seq dataset captures global transcriptomic changes in the rat bladder at multiple time points following spinal cord injury (SCI). Full-thickness bladder tissues were collected from male Sprague Dawley rats at 2, 8, and 16 weeks post-complete T8 spinal cord transection, alongside non-injured controls.
2025-07-09 | GSE294927 | GEO
Project description:To comprehensively elucidate metabolite changes in different anatomical structures (e.g., gray matter and white matter) after spinal cord injury(SCI), our study utilized air-flow-assisted desorption electrospray ionization mass spectrometry imaging platforms to perform untargeted metabolomic studies. These analyzes are designed to identify metabolites critical in spinal cord injury. confirmed the profile differences in white and gray matter as well as in ventral and dorsal horns after SCI. These results provide valuable information for understanding in situ metabolite alterations after SCI.
2025-03-28 | PXD060179 | Pride
Project description:The quantitative variations and specific roles of regulatory T cells (Treg cells) within spinal cord injury (SCI) remain elusive. Utilizing single-cell RNA sequencing, flow cytometry, and immunofluorescence, we discovered that Treg cells began to infiltrate the injured spinal cords in mice approximately three days after SCI. Selective depletion of Treg cells resulted in an expansion of the injury area, reduction in neuronal survival, and a decrease in long-term functional recovery post-SCI. Transcriptomic analyses of Treg cells unveiled potent anti-inflammatory functions and the potential to influence neighboring immune cells within the spinal cord after SCI. Adoptive transfer of Treg cells demonstrated measurable improvement in SCI recovery and increased neuronal retention in mice. However, selective depletion of microglia inhibited the neuroprotective effects of Treg cells, indicating that the effect of Treg cells in the spinal cord depends on the presence of microglia. Mechanistically, Treg cells promoted spinal cord functional recovery by upregulating microglial Abcg1 receptor expression, enhancing cholesterol transport, reducing microglial lipid droplet formation, and moderating the M1 phenotype after SCI. In summary, our study elucidates the spatiotemporal distribution of Treg cells after SCI and their unique transcriptomic features, clarifying the impact of Treg cells on microglial cholesterol metabolism and inflammatory phenotype. These findings indicate that Treg cells may serve as a potential target for SCI treatment.
2025-09-29 | GSE243607 | GEO
Project description:We have previously shown that Il1a-knockout (KO) mice exhibit rapid (at day 1) and persistent improvements in locomotion associated with reduced lesion volume compared with Il1b-KO mice and C57BL/6 controls after traumatic spinal cord injury (SCI). To investigate the mechanism by which Il1a mediates its detrimental effect, we analyzed the transcriptome of the injured spinal cord of Il1a-KO, Il1b-KO and C57BL/6 mice at 24 hours after SCI using GeneChip microarrays. Il1a-KO, Il1b-KO and C57BL/6 mice were subjected to a 50-kdyn SCI and a 6-mm spinal cord segment centered over the site of contusion extracted for RNA isolation and microarray analysis.
2015-06-27 | E-GEOD-70302 | biostudies-arrayexpress
Project description:Although axon regeneration can now be induced experimentally across anatomically complete spinal cord injury (SCI), restoring meaningful function after such injuries has been elusive. This failure contrasts with the spontaneous, naturally occuring repair that restores walking after severe but incomplete SCI. Here, we applied projection-specific and comparative single-nucleus RNA sequencing to uncover the transcriptional phenotype and connectome of neuronal subpopulations involved in natural spinal cord repair. We identified a molecularly defined population of excitatory projection neurons in the thoracic spinal cord that extend axons to the lumbar spinal cord where walking execution centers reside. We show that regrowing axons from these specific neurons across anatomically complete SCI and guiding them to reconnect with their appropriate target region in the lumbar spinal cord restores walking in mice. These results demonstrate that mechanism-based repair strategies that recapitulate the natural topology of molecularly defined neuronal subpopulations can restore neurological functions. Expanding this principle to different classes of neurons across the central nervous system may unlock the framework to achieve complete repair of the injured spinal cord.
2023-09-20 | GSE198949 | GEO
Project description:Summary: Spinal cord injury (SCI) is a damage to the spinal cord induced by trauma or disease resulting in a loss of mobility or feeling. SCI is characterized by a primary mechanical injury followed by a secondary injury in which several molecular events are altered in the spinal cord often resulting in loss of neuronal function. Analysis of the areas directly (spinal cord) and indirectly (raphe and sensorimotor cortex) affected by injury will help understanding mechanisms of SCI. Hypothesis: Areas of the brain primarily affected by spinal cord injury are the Raphe and the Sensorimotor cortex thus gene expression profiling these two areas might contribute understanding the mechanisms of spinal cord injury. Specific Aim: The project aims at finding significantly altered genes in the Raphe and Sensorimotor cortex following an induced moderate spinal cord injury in T9. Keywords: other
2005-02-11 | GSE2270 | GEO