ArticleFrontiers in genetics2022
Single-Cell RNA Sequencing Reveals Cellular and Transcriptional Changes Associated With Traumatic Brain Injury.
Article in Frontiers in genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Mild and repetitive mild traumatic brain injury: Changes in microglial cells and synapses.Neural regeneration research · 2026Article
- Traumatic Brain Injury and the Road to Alzheimer's Disease.Biomedicines · 2026Review
- Th17 cells and IL-17A in traumatic brain injury: mechanisms and therapeutic perspectives.Frontiers in immunology · 2026Review
- A single mild closed-head injury disrupts synaptic strength and promotes hippocampal hyperexcitability in mice.Brain communications · 2026Article
- Multi-omics profiling uncovers LINC00486-associated lncRNA regulation in human traumatic brain injury.Genes & genomics · 2026Article
- Spatiotemporal dynamics of neuronal subtypes and their interactions with glia following intracortical electrode implantation.Biology direct · 2025Article
- Astrocyte activation persists one year after TBI: a dynamic shift from inflammation to neurodegeneration.Communications biology · 2025Article
- Intranasal delivery of hypoxia-preconditioned extracellular vesicles derived from BMSCs alleviates neuroinflammation and brain dysfunction in TBI.Stem cell research & therapy · 2025Article
- Oxiracetam ameliorates neurological function after traumatic brain injury through competing endogenous RNA regulatory network.Psychopharmacology · 2025Article
- Altered Neuroinflammatory Transcriptomic Profile in the Hippocampal Dentate Gyrus Three Weeks After Lateral Fluid Percussion Injury in Rats.International journal of molecular sciences · 2025Article
- Review
- Single cell RNA sequencing after moderate traumatic brain injury: effects of therapeutic hypothermia.Journal of neuroinflammation · 2025Article
- High-altitude hypoxia aggravated neurological deficits in mice induced by traumatic brain injury via BACH1 mediating astrocytic ferroptosis.Cell death discovery · 2025Article
- Single-Cell RNA-Seq Reveals the Pseudo-temporal Dynamic Evolution Characteristics of ADSCs to Neuronal Differentiation.Cellular and molecular neurobiology · 2024Article
- Article
- Exploratory assessment of the effect of systemic administration of soluble glycoprotein 130 on cognitive performance and chemokine levels in a mouse model of experimental traumatic brain injury.Journal of neuroinflammation · 2024Article
- The contribution of the meningeal immune interface to neuroinflammation in traumatic brain injury.Journal of neuroinflammation · 2024Review
- Transcriptomic alterations in cortical astrocytes following the development of post-traumatic epilepsy.Scientific reports · 2024Article
- Strain in the Midbrain: Impact of Traumatic Brain Injury on the Central Serotonin System.Brain sciences · 2024Review
- Integration of clinical characteristics and molecular signatures of the tumor microenvironment to predict the prognosis of neuroblastoma.Journal of molecular medicine (Berlin, Germany) · 2023Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) is currently a substantial public health problem and one of the leading causes of morbidity and mortality worldwide. However, the cellular and transcriptional changes in TBI at single-cell level have not been well characterized. In this study, we reanalyzed a single-cell RNA sequencing (scRNA-seq) dataset of mouse hippocampus to identify the key cellular and transcriptional changes associated with TBI. Specifically, we found that oligodendrocytes were the most abundant cell type in mouse hippocampus, and detected an expanded astrocyte population, which was significantly activated in TBI. The enhanced activity of inflammatory response-related pathways in the astrocytes of TBI samples suggested that the astrocytes, along with microglia, which were the major brain-resident immune cells, were responsible for inflammation in the acute phase of TBI. Hormone secretion, transport, and exocytosis were found upregulated in the excitatory neurons of TBI, which gave us a hint that excitatory neurons might excessively transport and excrete glutamate in response to TBI. Moreover, the ependymal subpopulation C0 was TBI-specific and characterized by downregulated cilium movement, indicating that the attenuated activity of cilium movement following TBI might decrease cerebrospinal fluid flow. Furthermore, we observed that downregulated genes in response to candesartan treatment were preferentially expressed in excitatory neurons and were related to pathways like neuronal systems and neuroactive ligand-receptor interaction, indicating that candesartan might promote recovery of neurons after traumatic brain injury
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