Regional and age-related diversity of human mature oligodendrocytes.
Moein YaqubiJulia Xiao Xuan LuoSalma BaigQiao-Ling CuiKevin PetreccaHaritha DesuCatherine LarochelleElia AfanasievJeffery A HallRoy DudleyMyriam SrourLisbet HaglundJean OuelletMiltiadis GeorgiopoulosCarlo SantaguidaJoshua A SonnenLuke Michael HealyJo Anne StrattonTimothy E KennedyJack P AntelPublished in: Glia (2022)
Morphological and emerging molecular studies have provided evidence for heterogeneity within the oligodendrocyte population. To address the regional and age-related heterogeneity of human mature oligodendrocytes (MOLs) we applied single-cell RNA sequencing to cells isolated from cortical/subcortical, subventricular zone brain tissue samples, and thoracolumbar spinal cord samples. Unsupervised clustering of cells identified transcriptionally distinct MOL subpopulations across regions. Spinal cord MOLs, but not microglia, exhibited cell-type-specific upregulation of immune-related markers compared to the other adult regions. SVZ MOLs showed an upregulation of select number of development-linked transcription factors compared to other regions; however, pseudotime trajectory analyses did not identify a global developmental difference. Age-related analysis of cortical/subcortical samples indicated that pediatric MOLs, especially from under age 5, retain higher expression of genes linked to development and to immune activity with pseudotime analysis favoring a distinct developmental stage. Our regional and age-related studies indicate heterogeneity of MOL populations in the human CNS that may reflect developmental and environmental influences.
Keyphrases
- single cell
- spinal cord
- endothelial cells
- rna seq
- induced apoptosis
- poor prognosis
- white matter
- transcription factor
- induced pluripotent stem cells
- neuropathic pain
- cell cycle arrest
- pluripotent stem cells
- cell proliferation
- high throughput
- spinal cord injury
- gene expression
- inflammatory response
- machine learning
- signaling pathway
- blood brain barrier
- cell death
- dna methylation
- endoplasmic reticulum stress
- dna binding
- genome wide identification
- subarachnoid hemorrhage
- binding protein