ArticleMolecular neurobiology2014
Rat cerebellar slice cultures exposed to bilirubin evidence reactive gliosis, excitotoxicity and impaired myelinogenesis that is prevented by AMPA and TNF-α inhibitors.
Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Bilirubin in Parkinson's disease: pathogenic mechanisms and therapeutic potentials.Frontiers in neuroscience · 2026Review
- Transcriptomic and Proteomic Changes in the Brain Along with Increasing Phenotypic Severity in a Rat Model of Neonatal Hyperbilirubinemia.International journal of molecular sciences · 2025Article
- Molecular events in brain bilirubin toxicity revisited.Pediatric research · 2024Review
- Article
- Models of bilirubin neurological damage: lessons learned and new challenges.Pediatric research · 2023Review
- Effects of bilirubin on the development and electrical activity of neural circuits.Frontiers in cellular neuroscience · 2023Review
- Hyperbilirubinemia after surgical repair for acute type a aortic dissection: A propensity score-matched analysis.Frontiers in physiology · 2022Article
- Risk factors analysis of hyperbilirubinemia after off-pump coronary artery bypass grafting: a retrospective observational study.Journal of cardiothoracic surgery · 2021Observational
- Human IPSC-Derived Model to Study Myelin Disruption.International journal of molecular sciences · 2021Article
- Human Oligodendrocytes and Myelin In Vitro to Evaluate Developmental Neurotoxicity.International journal of molecular sciences · 2021Review
- Time to peak bilirubin concentration and advanced AKI were associated with increased mortality in rheumatic heart valve replacement surgery patients with severe postoperative hyperbilirubinemia: a retrospective cohort study.BMC cardiovascular disorders · 2021Article
- Severe postoperative hyperbilirubinemia in congenital heart disease.Open medicine (Warsaw, Poland) · 2021Article
- Curcumin Prevents Cerebellar Hypoplasia and Restores the Behavior in Hyperbilirubinemic Gunn Rat by a Pleiotropic Effect on the Molecular Effectors of Brain Damage.International journal of molecular sciences · 2020Article
- Characteristics and outcomes of Stanford type A aortic dissection patients with severe post-operation hyperbilirubinemia: a retrospective cohort study.Journal of cardiothoracic surgery · 2020Article
- Developmental Changes in Oligodendrocyte Genesis, Myelination, and Associated Behavioral Dysfunction in a Rat Model of Intra-generational Protein Malnutrition.Molecular neurobiology · 2019Article
- Embracing oligodendrocyte diversity in the context of perinatal injury.Neural regeneration research · 2017Review
- Evaluation of region selective bilirubin-induced brain damage as a basis for a pharmacological treatment.Scientific reports · 2017Article
- A Hypothesis for Using Pathway Genetic Load Analysis for Understanding Complex Outcomes in Bilirubin Encephalopathy.Frontiers in neuroscience · 2016Article
- The Blockade of NF-κB Activation by a Specific Inhibitory Peptide Has a Strong Neuroprotective Role in a Sprague-Dawley Rat Kernicterus Model.The Journal of biological chemistry · 2015Article
- Dexmedetomidine Attenuates Bilirubin-Induced Lung Alveolar Epithelial Cell Death In Vitro and In Vivo.Critical care medicine · 2015Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cerebellum is one of the most affected brain regions in the course of bilirubin-induced neurological dysfunction. We recently demonstrated that unconjugated bilirubin (UCB) reduces oligodendrocyte progenitor cell (OPC) survival and impairs oligodendrocyte (OL) differentiation and myelination in co-cultures of dorsal root ganglia neurons and OL. Here, we used organotypic cerebellar slice cultures, which replicate many aspects of the in vivo system, to dissect myelination defects by UCB in the presence of neuroimmune-related glial cells. Our results demonstrate that treatment of cerebellar slices with UCB reduces the number of myelinated fibres and myelin basic protein mRNA expression. Interestingly, UCB addition to slices increased the percentage of OPC and decreased mature OL content, whereas it decreased Olig1 and increased Olig2 mRNA expression. These UCB effects were associated with enhanced gliosis, revealed by an increased burden of both microglia and astrocytes. Additionally, UCB treatment led to a marked increase of tumor necrosis factor (TNF)-α and glutamate release, in parallel with a decrease of interleukin (IL)-6. No changes were observed relatively to IL-1β and S100B secretion. Curiously, both α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist and TNF-α antibody partially prevented the myelination defects that followed UCB exposure. These data point to a detrimental role of UCB in OL maturation and myelination together with astrocytosis, microgliosis, and both inflammatory and excitotoxic responses, which collectively may account for myelin deficits following moderate to severe neonatal jaundice.
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