Author Correction: Single-nucleus profiling of adult mice sub-ventricular zone after blast-related traumatic brain injury.
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ABSTRACT:
SUBMITTER: Li M
PROVIDER: S-EPMC10545782 | biostudies-literature | 2023 Oct
REPOSITORIES: biostudies-literature
Publications
Author Correction: Single-nucleus profiling of adult mice sub-ventricular zone after blast-related traumatic brain injury.
Li Manrui M Chen Xiameng X Yang Qiuyun Q Cao Shuqiang S Wyler Steven S Yuan Ruixuan R Zhang Lingxuan L Liao Miao M Lv Meili M Wang Feng F Guo Yadong Y Zhou Jihong J Zhang Lin L Xie Xiaoqi X Liang Weibo W
Scientific data 20231002 1
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Project description:Explosive blast-related traumatic brain injuries (bTBI) are common in war zones and urban terrorist attacks. These bTBIs often result in complex neuropathologic damage and neurologic complications. However, there is still a lack of specific strategies for diagnosing and/or treating bTBIs. The sub-ventricular zone (SVZ), which undergoes adult neurogenesis, is critical for the neurological maintenance and repair after brain injury. However, the cellular responses and mechanisms that trigger and modulate these activities in the pathophysiological processes following bTBI remain poorly understood. Here we employ single-nucleus RNA-sequencing (snRNA-seq) of the SVZ from mice subjected to a bTBI. This data-set, including 15272 cells (7778 bTBI and 7494 control) representing all SVZ cell types and is ideally suited for exploring the mechanisms underlying the pathogenesis of bTBIs. Additionally, it can serve as a reference for future studies regarding the diagnosis and treatment of bTBIs.
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Project description:To elucidate molecular features of the cells of Sub-ventricular Zone (SVZ), their progeny at each differentiation stage, and surrounding cells in SVZ under blast wave-induced changes, cells were profiled from matched SVZ of 3 mice that had received blast injury and 3 controls（The controls sequencing profile can be assessed in GEO at GSM5938054）.Cell type specific gene expression responding to (blast-related traumatic brain injury, bTBI) were revealed, some of which were closely associated with pathogenesis post-injury. Furthermore, the diverse cell to cell interaction networks uncovered an array of cellular processes under bTBI. Our gene expression atlas provides extensive resources for future researches regarding bTBI induced pathogenesis, its therapeutic interventions or diagnostic tests.
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Project description:Long-term molecular changes in the brain resulting from blast exposure may be mediated by epigenetic changes, such as deoxyribonucleic acid (DNA) methylation, that regulate gene expression. Aberrant regulation of gene expression is associated with behavioral abnormalities, where DNA methylation bridges environmental signals to sustained changes in gene expression. We assessed DNA methylation changes in the brains of rats exposed to three 74.5 kPa blast overpressure events, conditions that have been associated with long-term anxiogenic manifestations weeks or months following the initial exposures. Rat frontal cortex eight months post-exposure was used for cell sorting of whole brain tissue into neurons and glia. We interrogated DNA methylation profiles in these cells using Expanded Reduced Representation Bisulfite Sequencing. We obtained data for millions of cytosines, showing distinct methylation profiles for neurons and glia and an increase in global methylation in neuronal versus glial cells (p<10(-7)). We detected DNA methylation perturbations in blast overpressure-exposed animals, compared with sham blast controls, within 458 and 379 genes in neurons and glia, respectively. Differentially methylated neuronal genes showed enrichment in cell death and survival and nervous system development and function, including genes involved in transforming growth factor β and nitric oxide signaling. Functional validation via gene expression analysis of 30 differentially methylated neuronal and glial genes showed a 1.2 fold change in gene expression of the serotonin N-acetyltransferase gene (Aanat) in blast animals (p<0.05). These data provide the first genome-based evidence for changes in DNA methylation induced in response to multiple blast overpressure exposures. In particular, increased methylation and decreased gene expression were observed in the Aanat gene, which is involved in converting serotonin to the circadian hormone melatonin and is implicated in sleep disturbance and depression associated with traumatic brain injury.
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Project description:As a significant type of traumatic brain injury (TBI), blast-induced traumatic brain injury (bTBI) frequently results in severe neurological and psychological impairments. Due to its unique mechanistic and clinical features, bTBI presents diagnostic and therapeutic challenges compared to other TBI forms. The hippocampus, an important site for secondary injury of bTBI, serves as a key niche for neural regeneration and repair post-injury, and is closely associated with the neurological outcomes of bTBI patients. Nonetheless, the pathophysiological alterations of hippocampus underpinning bTBI remain enigmatic, and a corresponding transcriptomic dataset for research reference is yet to be established. In this investigation, the single-nucleus RNA sequencing (snRNA-seq) technique was employed to sequence individual hippocampal nuclei of mice from bTBI and sham group. Upon stringent quality control, gene expression data from 17,278 nuclei were obtained, with the dataset's reliability substantiated through various analytical methods. This dataset holds considerable potential for exploring secondary hippocampal injury and neurogenesis mechanisms following bTBI, with important reference value for the identification of specific diagnostic and therapeutic targets for bTBI.
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Project description:The subventricular zone (SVZ) is a neurogenetic niche that contributes to homeostasis and repair after brain injury. However, effects of mild traumatic brain injury (mTBI) on genomewide gene expression in the SVZ remain largely unexplored. To address this issue, we investigated the single-nucleus transcriptomic profiles of the SVZ after mTBI. 18 distinct clusters were yielded via unsupervised clustering of the transcriptomic profiles. Cell type specific gene expression responding to mTBI were revealed, some of which were closely associated with pathogenesis post-injury. Furthermore, the diverse cell to cell interaction networks uncovered an array of cellular processes under mTBI. Also, we reported novel lineage trajectories and molecular hallmarks that govern the neurogenesis. Our gene expression atlas provides extensive resources for future researches regarding mTBI induced pathogenesis, its therapeutic interventions or diagnostic tests.
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Project description:The production of neurons from neural stem cells (NSCs) persists throughout life in the mouse ventricular-subventricular zone (V-SVZ). We have previously reported that NSCs from adult V-SVZ are contained in cell populations expressing the carbohydrate SSEA-1/LeX, which exhibit either characteristics of quiescent NSCs (qNSCs) or of actively dividing NSCs (aNSCs) based on the absence or the presence of EGF-receptor, respectively. Using the fluorescence ubiquitination cell cycle indicator-Cdt1 transgenic mice to mark cells in G0/G1 phase of the cell cycle, we uncovered a subpopulation of qNSCs which were primed to enter the cell cycle in vitro. Besides, we found that treatment with Syndecan-1, a heparan sulfate proteoglycan involved in NSC proliferation, hastened the division of qNSCs and increased proliferation of aNSCs shortening their G1 phase in vitro. Furthermore, administration of Syndecan-1 ameliorated the recovery of neurogenic populations in the V-SVZ after radiation-induced injury providing potential cure for neurogenesis decline during brain aging or after injury.
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