ArticleCNS neuroscience & therapeutics2023
Single-cell RNA-sequencing analysis reveals enhanced non-canonical neurotrophic factor signaling in the subacute phase of traumatic brain injury.
Article in CNS neuroscience & therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Single-cell RNA sequencing in stroke and traumatic brain injury: Current achievements, challenges and future perspectives on transcriptomic profiling.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
- Single-nucleus analysis reveals human-specific oligodendrocyte polarization and conserved neuronal responses after severe traumatic brain injury.Nature communications · 2026Article
- Spatial Transcriptomics and Dual Dye Mapping Identify Wnt-Driven BBB Protection in Endothelial EphA4-Deficiency.Research square · 2026Article
- Midkine Overexpression Promotes Functional Recovery After Spinal Cord Injury by Enhancing Microglial Efferocytosis Via LRP-1.CNS neuroscience & therapeutics · 2026Article
- Prosaposin in CNS health and disease, metabolic stress and exercise adaptation.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Th17 cells and IL-17A in traumatic brain injury: mechanisms and therapeutic perspectives.Frontiers in immunology · 2026Review
- Stress-Induced Activation of Prolactin-NR4A1-Midkine Axis Exacerbates Skin Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The roles of pleiotrophin in brain injuries: a narrative review of the literature.Annals of medicine · 2025Review
- Neuroprotective effects of cobalt oxide nanoparticles through mitigating oxidative stress and reactive glial responses in traumatic brain injury.Materials today. Bio · 2025Article
- Single cell RNA sequencing after moderate traumatic brain injury: effects of therapeutic hypothermia.Journal of neuroinflammation · 2025Article
- Astrocytic pleiotrophin deficiency in the prefrontal cortex contributes to stress-induced depressive-like responses in male mice.Nature communications · 2025Article
- High-altitude hypoxia aggravated neurological deficits in mice induced by traumatic brain injury via BACH1 mediating astrocytic ferroptosis.Cell death discovery · 2025Article
- Thyroid hormone T4 mitigates traumatic brain injury in mice by dynamically remodeling cell type specific genes, pathways, and networks in hippocampus and frontal cortex.Biochimica et biophysica acta. Molecular basis of disease · 2024Article
- Article
- Mgp High-Expressing MSCs Orchestrate the Osteoimmune Microenvironment of Collagen/Nanohydroxyapatite-Mediated Bone Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Reactive gliosis in traumatic brain injury: a comprehensive review.Frontiers in cellular neuroscience · 2024Review
- Single-cell RNA-sequencing analysis reveals enhanced non-canonical neurotrophic factor signaling in the subacute phase of traumatic brain injury.CNS neuroscience & therapeutics · 2023Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTraumatic brain injury (TBI) is a leading cause of long-term disability in young adults and induces complex neuropathological processes. Cellular autonomous and intercellular changes during the subacute phase contribute substantially to the neuropathology of TBI. However, the underlying mechanisms remain elusive. In this study, we explored the dysregulated cellular signaling during the subacute phase of TBI.
methodsSingle-cell RNA-sequencing data (GSE160763) of TBI were analyzed to explore the cell-cell communication in the subacute phase of TBI. Upregulated neurotrophic factor signaling was validated in a mouse model of TBI. Primary cell cultures and cell lines were used as in vitro models to examine the potential mechanisms affecting signaling.
resultsSingle-cell RNA-sequencing analysis revealed that microglia and astrocytes were the most affected cells during the subacute phase of TBI. Cell-cell communication analysis demonstrated that signaling mediated by the non-canonical neurotrophic factors midkine (MDK), pleiotrophin (PTN), and prosaposin (PSAP) in the microglia/astrocytes was upregulated in the subacute phase of TBI. Time-course profiling showed that MDK, PTN, and PSAP expression was primarily upregulated in the subacute phase of TBI, and astrocytes were the major source of MDK and PTN after TBI. In vitro studies revealed that the expression of MDK, PTN, and PSAP in astrocytes was enhanced by activated microglia. Moreover, MDK and PTN promoted the proliferation of neural progenitors derived from human-induced pluripotent stem cells (iPSCs) and neurite growth in iPSC-derived neurons, whereas PSAP exclusively stimulated neurite growth.
conclusionThe non-canonical neurotrophic factors MDK, PTN, and PSAP were upregulated in the subacute phase of TBI and played a crucial role in neuroregeneration.
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