ArticleMolecular neurobiology2013
Unconjugated bilirubin restricts oligodendrocyte differentiation and axonal myelination.
Article in Molecular neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 40 citations in OpenAlex.
- Hyperbilirubinemia and phototherapy differentially alter hippocampal transcriptome in the preterm Gunn rat model.Pediatric research · 2026Article
- Timed fetal inflammation and postnatal hypoxia cause cortical white matter injury, interneuron imbalances, and behavioral deficits in a double-hit rat model of encephalopathy of prematurity.Brain, behavior, & immunity - health · 2024Article
- Molecular events in brain bilirubin toxicity revisited.Pediatric research · 2024Review
- Effects of bilirubin on the development and electrical activity of neural circuits.Frontiers in cellular neuroscience · 2023Review
- Bilirubin Encephalopathy.Current neurology and neuroscience reports · 2022Review
- Review of bilirubin neurotoxicity I: molecular biology and neuropathology of disease.Pediatric research · 2020Review
- Developmental Changes in Oligodendrocyte Genesis, Myelination, and Associated Behavioral Dysfunction in a Rat Model of Intra-generational Protein Malnutrition.Molecular neurobiology · 2019Article
- Histone acetylation as a new mechanism for bilirubin-induced encephalopathy in the Gunn rat.Scientific reports · 2018Article
- Neuroinflammation and ER-stress are key mechanisms of acute bilirubin toxicity and hearing loss in a mouse model.PloS one · 2018Article
- Embracing oligodendrocyte diversity in the context of perinatal injury.Neural regeneration research · 2017Review
- Developmental, Genetic, Dietary, and Xenobiotic Influences on Neonatal Hyperbilirubinemia.Molecular pharmacology · 2017Review
- Key Aging-Associated Alterations in Primary Microglia Response to Beta-Amyloid Stimulation.Frontiers in aging neuroscience · 2017Article
- Reduced Myelination and Increased Glia Reactivity Resulting from Severe Neonatal Hyperbilirubinemia.Molecular pharmacology · 2016Article
- Exploring New Inflammatory Biomarkers and Pathways during LPS-Induced M1 Polarization.Mediators of inflammation · 2016Article
- A Hypothesis for Using Pathway Genetic Load Analysis for Understanding Complex Outcomes in Bilirubin Encephalopathy.Frontiers in neuroscience · 2016Article
- The role of the surface on microglia function: implications for central nervous system tissue engineering.Journal of the Royal Society, Interface · 2015Article
- Intracellular alpha-synuclein affects early maturation of primary oligodendrocyte progenitor cells.Molecular and cellular neurosciences · 2014Article
- Hemoglobin as a source of iron overload in multiple sclerosis: does multiple sclerosis share risk factors with vascular disorders?Cellular and molecular life sciences : CMLS · 2014Article
- Rat cerebellar slice cultures exposed to bilirubin evidence reactive gliosis, excitotoxicity and impaired myelinogenesis that is prevented by AMPA and TNF-α inhibitors.Molecular neurobiology · 2014Article
- Microglia change from a reactive to an age-like phenotype with the time in culture.Frontiers in cellular neuroscience · 2014Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
High levels of serum unconjugated bilirubin (UCB) in newborns are associated with axonal damage and glial reactivity that may contribute to subsequent neurologic injury and encephalopathy (kernicterus). Impairments in myelination and white matter damage were observed at autopsy in kernicteric infants. We have recently reported that UCB reduces oligodendrocyte progenitor cell (OPC) survival in a pure OPC in vitro proliferative culture. Here, we hypothesized that neonatal hyperbilirubinemia may also impair oligodendrocyte (OL) maturation and myelination. We used an experimental model of hyperbilirubinemia that has been shown to mimic the pathophysiological conditions leading to brain dysfunction by unbound (free) UCB. Using primary cultures of OL, we demonstrated that UCB delays cell differentiation by increasing the OPC number and reducing the number of mature OL. This finding was combined with a downregulation of Olig1 mRNA levels and upregulation of Olig2 mRNA levels. Addition of UCB, prior to or during differentiation, impaired OL morphological maturation, extension of processes and cell diameter. Both conditions reduced active guanosine triphosphate (GTP)-bound Rac1 fraction. In myelinating co-cultures of dorsal root ganglia neurons and OL, UCB treatment prior to the onset of myelination decreased oligodendroglial differentiation and the number of myelinating OL, also observed when UCB was added after the onset of myelination. In both circumstances, UCB decreased the number of myelin internodes per OL, as well as the myelin internode length. Our studies demonstrate that increased concentrations of UCB compromise myelinogenesis, thereby elucidating a potential deleterious consequence of elevated UCB.
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