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Cited by 12Autophagy in Disease and TherapyCalcium signaling and nucleotide metabolismCellular transport and secretion

Assessment and Quantification of Crystal-Induced Lysosomal Damage

Duewell, Peter, Latz, Eicke·2013·Methods in Molecular Biology
DOI 10.1007/978-1-62703-523-1_3
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Abstract

Lysosomes are organelles that degrade endocytosed, phagocytosed, or autophagocytosed materials. Lysosomal degradation of engulfed material is a highly controlled mechanism, which is vital in the control of infection, recycling of cellular organelles, and the breakdown of larger material. Following ingestion, lysosomes acidify and mature, leading to the activation of a range of proteolytic enzymes. Lysosomes are considered stable organelles that separate their highly hydrolytic enzymes from the cytosol to prevent digestion of self-molecules and host cell damage. Some substances, mostly of a particulate or aggregated nature, are able to damage lysosomes. Lysosomal damage and rupture, with subsequent release of lysosomal content into the cytosol can have dramatic consequences for the cell, such as the induction of cell death or activation of the NLRP3 inflammasome. In this chapter, we provide methods for the induction, assessment, and quantification of lysosomal damage by flow cytometry and confocal microscopy.

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Crossref · 10.1007/978-1-62703-523-1_3

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  • OxLDL primes and activates the NLRP3 inflammasome in macrophages in mouse models of atherosclerosis: it primes via the CD36-TLR4-TLR6 complex and, after lysosomal transport, activates via cholesterol crystallization and lysosomal damage.

    “OxLDL has been shown both to prime and to activate the NLRP3 inflammasome in macrophages in mouse models of atherosclerosis: first, oxLDL primes the NLRP3 inflammasome by binding to the CD36–TLR4–TLR6 signalling complex on the macrophage surface and, then, after having been transported to lysosomes, the oxLDL activates the NLRP3 inflammasome via induction of cholesterol crystallization and ensuing”

    From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [71]

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Authors
Duewell, P., & Latz, E.
Affiliations
  • LMU Klinikum (DE)
  • University of Bonn (DE)
ORCID
Venue
Methods in Molecular Biology
Publisher
Humana Press
Published
2013
Volume
1040
Pages
19-27
ISSN
  • 1064-3745 (ISSN-L)
  • 1940-6029
DOI
10.1007/978-1-62703-523-1_3
OpenAlex
W124277487
Cited by
12
References
4
Citations by year
2026: 1 · 2025: 2 · 2021: 3 · 2019: 4 · 2018: 1 · 2014: 1
FWCI
1.36
Type
book chapter
Language
en
Open access
closed
Locations
  • Methods in molecular biology (publishedVersion)
  • PubMed (publishedVersion)
  • DZNE Pub (submittedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
Keywords
lysosomal damage, lysosomal rupture, NLRP3 inflammasome, cell death, lysosomal acidification, flow cytometry, confocal microscopy, lysosomal degradation
MeSH terms
Animals, Biological Transport, Crystallins, Flow Cytometry, Lysosomes, Macrophages, Microscopy, Confocal, Liquid Crystals, Mice

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