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Sensitivity to Lysosome-Dependent Cell Death Is Directly Regulated by Lysosomal Cholesterol Content
Open accessAbstract
Alterations in lipid homeostasis are implicated in several neurodegenerative diseases, although the mechanisms responsible are poorly understood. We evaluated the impact of cholesterol accumulation, induced by U18666A, quinacrine or mutations in the cholesterol transporting Niemann-Pick disease type C1 (NPC1) protein, on lysosomal stability and sensitivity to lysosome-mediated cell death. We found that neurons with lysosomal cholesterol accumulation were protected from oxidative stress-induced apoptosis. In addition, human fibroblasts with cholesterol-loaded lysosomes showed higher lysosomal membrane stability than controls. Previous studies have shown that cholesterol accumulation is accompanied by the storage of lipids such as sphingomyelin, glycosphingolipids and sphingosine and an up regulation of lysosomal associated membrane protein-2 (LAMP-2), which may also influence lysosomal stability. However, in this study the use of myriocin and LAMP deficient fibroblasts excluded these factors as responsible for the rescuing effect and instead suggested that primarily lysosomal cholesterol content determineD the cellular sensitivity to toxic insults. Further strengthening this concept, depletion of cholesterol using methyl-β-cyclodextrin or 25-hydroxycholesterol decreased the stability of lysosomes and cells became more prone to undergo apoptosis. In conclusion, cholesterol content regulated lysosomal membrane permeabilization and thereby influenced cell death sensitivity. Our data suggests that lysosomal cholesterol modulation might be used as a therapeutic strategy for conditions associated with accelerated or repressed apoptosis.
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“Moreover, under physiological conditions, lysosomal membranes can be stabilized by altering lysosomal cholesterol content [788] or by boosting endogenous activity of heat shock protein family A (Hsp70) member 1A (HSPA1A; best known as HSP70) [789, 790].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [788]
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Citations
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BackgroundResultInfluentialChronic exposure to U18666A induces apoptosis in cultured murine cortical neurons
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BackgroundMethodSelf-citation
Flagged first, then by citations
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“Perimeter membranes are protected by a thick glycocalyx enriched in polylactosamine structures, and by a high cholesterol level (Hay, 1989; Appelqvist et al., 2012), the chaperon HSP70 (Kirkegaard et al., 2010), and presumably also by a high lateral pressure attenuating the interaction with GM2AP,…”
Metadata
- Authors
- Appelqvist, H., Sandin, L., Björnström, K., Saftig, P., Garner, B., Öllinger, K., & Kågedal, K.
- Affiliations
- Linköping University (SE)
- University of Wollongong (AU)
- Corresponding author
- Appelqvist, Hanna
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2012-11-16
- Volume
- 7
- Issue
- 11
- Pages
- e50262
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3500374
- OpenAlex
- W2033615443
- Cited by
- 108
- References
- 46
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 8 · 2023: 13 · 2022: 5 · 2021: 13 · 2020: 14 · 2019: 4 · 2018: 4 · 2017: 6 · 2016: 9 · 2015: 7 · 2014: 7 · 2013: 9
- FWCI
- 4.93
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Research Online (University of Wollongong) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Figshare (submittedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- Vetenskapsrådet (2010-03463)
- Topics
- Health Sciences › Medicine › Genetics (clinical) › Lysosomal Storage Disorders Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Keywords
- lysosomal cholesterol, lysosome-dependent cell death, apoptosis, lysosomal membrane stability, lysosomal membrane permeabilization, Niemann-Pick disease type C1, NPC1 protein, cholesterol accumulation, lipid homeostasis, neurodegenerative diseases, oxidative stress, myriocin, methyl-β-cyclodextrin, 25-hydroxycholesterol, LAMP2, neurons, fibroblasts
- MeSH terms
- Niemann-Pick C1 Protein, Androstenes, Carrier Proteins, Cholesterol, Fibroblasts, Flow Cytometry, Humans, Hydroxycholesterols, Immunohistochemistry, Lysosomes, Membrane Glycoproteins, Microscopy, Phase-Contrast, Mutation, Neurons, Quinacrine, Blotting, Western, Cell Death, Statistics, Nonparametric, beta-Cyclodextrins, Intracellular Signaling Peptides and Proteins, Lysosomal Membrane Proteins
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