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Keywords {🔍}

cell, pubmed, cells, article, google, scholar, brain, injury, mtbi, types, cas, cortex, gene, hippocampus, frontal, tbi, genes, degs, central, fig, humanin, expression, acute, phase, traumatic, type, pathways, blood, supplementary, control, singlecell, astrocytes, tissue, timepoints, usa, subacute, sham, treatment, posttbi, peripheral, tissues, timepoint, mtrnr, table, molecular, study, number, immune, data, cellular,

Topics {✒️}

k-nearest-neighbor batch-effect test ligand–receptor-mediated cell–cell communication k-nearest neighbor matrix 2-deoxy-d-glucose autoradiographic study drop-seq single-cell barcoding ligand–receptor cell–cell communication cell-type-specific therapeutic interventions revealed numerous cell-type-specific drop-seq data pre-processing single-cell rna sequencing single-cell rna-seq cell-type-independent genes responsive fernando gomez-pinilla cell-type-specific markers curated cell-type-specific marker genes infer cell–cell communication edta-treated collection tubes saturated-fat diet aggravates cell-type-specific degs affected acceptor molecule n-acetylaspartate choroid plexus-csf nexus cell-type-specific degs identified serum-deprived human lymphocytes drop-seq tools v1 de kerchove d'exaerde drop-seq data reported nuclearly-encoded humanin isoforms central nervous system multi-timepoint systems-level investigation early maternal-fetal interface article download pdf age-dependent signaling differences ligand–peptide gene coregulation wilcoxon rank-sum test pro-inflammatory m-1 type query single-cell data 40 µg/1 kg body weight mt-rnr2 expression levels gelatin-coated histological slides online drop-seq protocol single-cell resolution study stages include mt-rnr2 mitochondrial-derived peptide humanin cell-type-specific degs tissue-specific eqtl files closed-head concussive injury background ambient mrna humanin-treated tbi animals mitochondrial gene mt-rnr2 illumina high-throughput sequencing

Questions {❓}

• Ariyannur PS, Arun P, Barry ES, Andrews-Shigaki B, Bosomtwi A, Tang H, Selwyn R, Grunberg NE, Moffett JR, Namboodiri AM (2013) Do reductions in brain N-acetylaspartate levels contribute to the etiology of some neuropsychiatric disorders?
• Burtscher J, Mallet RT, Burtscher M, Millet GP (2021) Hypoxia and brain aging: Neurodegeneration or neuroprotection?
• Gong Z, Tas E, Muzumdar R (2014) Humanin and age-related diseases: a new link?
• Keightley ML, Sinopoli KJ, Davis KD, Mikulis DJ, Wennberg R, Tartaglia MC, Chen JK, Tator CH (2014) Is there evidence for neurodegenerative change following traumatic brain injury in children and youth?
• Lee C, Yen K, Cohen P (2013) Humanin: a harbinger of mitochondrial-derived peptides?
• Our findings offer unparalleled insights into the spatiotemporal pathophysiology of mTBI by answering the following longstanding questions, such as: Which cell types, genes, and pathways are most sensitive to mTBI in a spatial- or temporal-specific manner?

Schema {🗺️}

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         headline:Systems spatiotemporal dynamics of traumatic brain injury at single-cell resolution reveals humanin as a therapeutic target
         description:The etiology of mild traumatic brain injury (mTBI) remains elusive due to the tissue and cellular heterogeneity of the affected brain regions that underlie cognitive impairments and subsequent neurological disorders. This complexity is further exacerbated by disrupted circuits within and between cell populations across brain regions and the periphery, which occur at different timescales and in spatial domains. We profiled three tissues (hippocampus, frontal cortex, and blood leukocytes) at the acute (24-h) and subacute (7-day) phases of mTBI at single-cell resolution. We demonstrated that the coordinated gene expression patterns across cell types were disrupted and re-organized by TBI at different timescales with distinct regional and cellular patterns. Gene expression-based network modeling implied astrocytes as a key regulator of the cell–cell coordination following mTBI in both hippocampus and frontal cortex across timepoints, and mt-Rnr2, which encodes the mitochondrial peptide humanin, as a potential target for intervention based on its broad regional and dynamic dysregulation following mTBI. Treatment of a murine mTBI model with humanin reversed cognitive impairment caused by mTBI through the restoration of metabolic pathways within astrocytes. Our results offer a systems-level understanding of the dynamic and spatial regulation of gene programs by mTBI and pinpoint key target genes, pathways, and cell circuits that are amenable to therapeutics.
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            name:University of California, Los Angeles
            address:
               name:Bioinformatics Interdepartmental Program, University of California, Los Angeles, Los Angeles, USA
               type:PostalAddress
            type:Organization
            name:University of California, Los Angeles
            address:
               name:Institute for Quantitative and Computational Biosciences, University of California, Los Angeles, Los Angeles, USA
               type:PostalAddress
            type:Organization
            name:University of California, Los Angeles
            address:
               name:Molecular Biology Institute, University of California, Los Angeles, Los Angeles, USA
               type:PostalAddress
            type:Organization
            name:University of California, Los Angeles
            address:
               name:Brain Research Institute, University of California, Los Angeles, Los Angeles, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, USA
      name:Bioinformatics Interdepartmental Program, University of California, Los Angeles, Los Angeles, USA
      name:Department of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, USA
      name:Department of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, USA
      name:Department of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, USA
      name:Department of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, USA
      name:Department of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, USA
      name:Department of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, USA
      name:Department of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, USA
      name:Department of Neurosurgery, University of California, Los Angeles, Los Angeles, USA
      name:Brain Injury Research Center, University of California, Los Angeles, Los Angeles, USA
      name:Department of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, USA
      name:Bioinformatics Interdepartmental Program, University of California, Los Angeles, Los Angeles, USA
      name:Institute for Quantitative and Computational Biosciences, University of California, Los Angeles, Los Angeles, USA
      name:Molecular Biology Institute, University of California, Los Angeles, Los Angeles, USA
      name:Brain Research Institute, University of California, Los Angeles, Los Angeles, USA

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