ArticlePediatric research2021
Bilirubin inhibits lipid raft dependent functions of L1 cell adhesion molecule in rat pup cerebellar granule neurons.
Article in Pediatric research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Label-Free Quantification of Bilirubin Using a Refractive Index-Insensitive Nanolaminate SERS Substrate.Biosensors · 2026Article
- EphB4-decorated biomimetic nanoparticles enhance osteoclast targeting and therapeutic effect in osteoporosis.Journal of nanobiotechnology · 2026Article
- Pleuromutilins Suppress Hepatocellular Carcinoma Growth via ABCA1 Inhibition-Induced Cholesterol Accumulation.Cancers · 2026Article
- Choline attenuates bilirubin induced effects on tyrosine phosphorylation and distribution in lipid rafts of L1 cell adhesion molecule in vivo.Pediatric research · 2026Article
- Choline supplementation mitigates effects of bilirubin in cerebellar granule neurons in vitro.Pediatric research · 2024Article
- Brain edema formation and therapy after intracerebral hemorrhage.Neurobiology of disease · 2023Review
- Neonatal hypoxia ischemia redistributes L1 cell adhesion molecule into rat cerebellar lipid rafts.Pediatric research · 2022Article
- Cholesterol in Brain Development and Perinatal Brain Injury: More than a Building Block.Current neuropharmacology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundThe mechanism of bilirubin neurotoxicity is poorly understood. We hypothesize that bilirubin inhibits the function of lipid rafts (LR), microdomains of the plasma membrane critical for signal transduction. To test this hypothesis, we measured the effect of free bilirubin (Bf) between 7.6 and 122.5 nM on LR-dependent functions of L1 cell adhesion molecule (L1).
methodsCerebellar granule neurons (CGN) were plated on poly-L-lysine overnight, and neurite length was determined after 1 h treatment with L1 alone or L1 and bilirubin. L1 activation of ERK1/2 was measured in CGN in the presence or absence of bilirubin. The effect of bilirubin on L1 distribution in LR was quantitated, and the localization of bilirubin to LR was determined.
resultsThe addition of bilirubin to CGN treated with L1 significantly decreased neurite length compared to L1 alone. L1 activation of ERK1/2 was inhibited by bilirubin. Bilirubin redistributed L1 into LR. Bilirubin was associated only with LR-containing fractions of a sucrose density gradient.
conclusionBf significantly inhibits LR-dependent functions of L1 and are found only associated with LR, suggesting one mechanism by which bilirubin may exert neurotoxicity is through the dysfunction of protein-LR interactions. IMPACT: This article establishes lipid rafts as a target for the neurotoxic effects of bilirubin. This article provides clear evidence toward establishing one mechanism of bilirubin neurotoxicity, where little is understood. This article paves the way for future investigation into lipid raft dependent functions, and its role in neurodevelopmental outcome.
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