ArticleCommunications biology2024
Lipid-nanoparticle-induced vacuolization in microglia.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Live cell imaging of exogenous α-synuclein fibrils in primary microglia and neuron co-cultures.Biochemistry and biophysics reports · 2026Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lipid-containing vacuoles in microglia were discovered more than one hundred years ago in the brain of patients showing neurodegenerative processes. Recently, molecular-biological studies demonstrated specific changes in lipid-metabolism related to neurodegeneration. Despite that already Alzheimer described a distinct glia phenotype having large, lipid-containing vacuoles (Gitterzellen), little is known about how microglia convert lipid metabolites into a vacuolated phenotype. We studied the impact of liver-derived, insoluble, lipid-enriched nanoparticles (Lef-NP) ( ~ 20 nm) and of ceramide-coated Percoll-nanoparticles (Cer-NP) ( ~ 20 nm) on vacuolization in microglia. Lipidomic analysis of Lef-NP revealed numerous distinct lipids, including pro-inflammatory ceramides, which are enriched in the brain of Alzheimer patients. Video microscopy revealed that hepatocyte-derived Lef-NP and Cer-NP enhanced macropinocytosis, followed by macropinosome swelling and formation of the Gitterzellen phenotype. Neither ceramide nor Percoll-nanoparticles induced Gitterzellen-formation. Electron-tomography visualized membrane contact-sites between nanoparticle-loaded endosomes, endoplasmic reticulum cisternae and mitochondria. Suppression of lipid-nanoparticle-induced Gitterzellen-formation by amiloride, which supresses macropinocytosis, and bafilomycin A, an endosomal acidification inhibitor, further confirmed a pinocytotic pathway in Gitterzellen-formation. Bafilomycin A also reversed Gitterzellen to a ramified microglia phenotype. Our experimental findings suggest that lipid-nanoparticles but not emulsified lipids provoke vacuolization in microglia, and provide a simple in-vitro model for a pathogenic process taking years in the human brain.
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