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Assessing Mitochondrial Function in Sciatic Nerve by High-Resolution Respirometry

Assessing Mitochondrial Function in Sciatic Nerve by High-Resolution Respirometry

Published on: May 5, 2022

Glucosylsphingosine affects mitochondrial function in a neuronal cell model.

Valeria Nikolaenko¹, Reddy Vootukuri¹, Simon Eaton²

¹Translational Mass Spectrometry Research Group, Genetics & Genomic Medicine Dept., UCL Institute of Child Health, London, WC1N 1EH, UK.

Communications Biology

|August 21, 2025

Summary

This summary is machine-generated.

High glucosylsphingosine levels in Gaucher disease impair cellular energy metabolism. This impacts the TCA cycle, glycolysis, and mitochondrial function, potentially contributing to disease pathology.

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Mitochondrial Preparation from Microglia for Glycan Analysis

Mitochondrial Preparation from Microglia for Glycan Analysis

Published on: May 30, 2025

Area of Science:

Biochemistry
Cell Biology
Neuroscience

Background:

Gaucher disease is caused by glucocerebrosidase mutations, leading to glucosylceramide accumulation and deacylation to glucosylsphingosine.
Glucocerebrosidase gene mutations are a significant genetic risk factor for Parkinson's disease.
Glucosylsphingosine is a Gaucher disease biomarker, but its toxic mechanisms are poorly understood.

Purpose of the Study:

To investigate the cellular effects of glucosylsphingosine at physiological concentrations found in Gaucher disease.
To elucidate the mechanisms underlying glucosylsphingosine toxicity in cellular models.

Main Methods:

Proteomics analysis of SH-Sy5y cells incubated with glucosylsphingosine.
Functional assays measuring ATP production, oxidative stress, and glycolysis.
Analysis of ubiquitinated proteins and lipid-binding studies.

Main Results:

Glucosylsphingosine negatively affects the TCA cycle, mitochondrial function, glycolysis, and protein ubiquitination.
Confirmed reduction in ATP production, increased oxidative stress, and enhanced glycolysis.
Demonstrated binding affinity for tubulin alpha and increased ubiquitination of alpha and beta tubulins.

Conclusions:

Supranormal glucosylsphingosine levels disrupt cellular energy metabolism.
These metabolic disturbances may contribute to the pathogenesis of Gaucher disease.
Glucosylsphingosine's interaction with tubulin warrants further investigation.