ArticleCell death and differentiation2017
Intrinsic repair protects cells from pore-forming toxins by microvesicle shedding.
Article in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 103 citations in OpenAlex.
- Vav2 is a master regulator of repair against bacterial pore-forming toxins.Life science alliance · 2026Article
- The ALS- and FTD-associated proteins annexin A11 and CHMP2B act sequentially in plasma membrane repair.Developmental cell · 2026Article
- Bacterial pore-forming toxins: mechanisms and implications for host immunity.Bioscience reports · 2026Review
- Stepwise assembly of α-hemolysin from intermediates to the mature pore in native erythrocytes.The Journal of cell biology · 2026Article
- The fungal peptide toxin candidalysin induces distinct membrane repair mechanisms compared to bacterial pore-forming toxins.Cell death discovery · 2025Article
- Interaction of an Oomycete Nep1-like Cytolysin with Natural and Plant Cell-Mimicking Membranes.The Journal of membrane biology · 2025Article
- Immune priming in the insect gut: a dynamic response revealed by ultrastructural and transcriptomic changes.BMC biology · 2025Article
- Calpains orchestrate secretion of annexin-containing microvesicles during membrane repair.The Journal of cell biology · 2025Article
- Epsilon Toxin fromToxins · 2024Article
- The epsilon toxin from Clostridium perfringens stimulates calcium-activated chloride channels, generating extracellular vesicles in Xenopus oocytes.Pharmacology research & perspectives · 2024Article
- LITAF protects against pore-forming protein-induced cell death by promoting membrane repair.Science immunology · 2024Article
- JAK/STAT signaling regulated intestinal regeneration defends insect pests against pore-forming toxins produced by Bacillus thuringiensis.PLoS pathogens · 2024Article
- Triply Enhanced Immunotherapy via Dual Glycan Reforming Integrated with Perforation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Aminopeptidase MNP-1 triggers intestine protease production by activating daf-16 nuclear location to degrade pore-forming toxins in Caenorhabditis elegans.PLoS pathogens · 2023Article
- Review
- Silver Nanoparticles Modified with Polygonatum sibiricum Polysaccharide Improve Biocompatibility and Infected Wound Bacteriostasis.Journal of microbiology (Seoul, Korea) · 2023Article
- Early Endosomes Act as Local Exocytosis Hubs to Repair Endothelial Membrane Damage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Patch repair protects cells from the small pore-forming toxin aerolysin.Journal of cell science · 2023Article
- Article
- Cholesterol-dependent cytolysins: The outstanding questions.IUBMB life · 2022Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pore-forming toxins (PFTs) are used by both the immune system and by pathogens to disrupt cell membranes. Cells attempt to repair this disruption in various ways, but the exact mechanism(s) that cells use are not fully understood, nor agreed upon. Current models for membrane repair include (1) patch formation (e.g., fusion of internal vesicles with plasma membrane defects), (2) endocytosis of the pores, and (3) shedding of the pores by blebbing from the cell membrane. In this study, we sought to determine the specific mechanism(s) that cells use to resist three different cholesterol-dependent PFTs: Streptolysin O, Perfringolysin O, and Intermedilysin. We found that all three toxins were shed from cells by blebbing from the cell membrane on extracellular microvesicles (MVs). Unique among the cells studied, we found that macrophages were 10 times more resistant to the toxins, yet they shed significantly smaller vesicles than the other cells. To examine the mechanism of shedding, we tested whether toxins with engineered defects in pore formation or oligomerization were shed. We found that oligomerization was necessary and sufficient for membrane shedding, suggesting that calcium influx and patch formation were not required for shedding. However, pore formation enhanced shedding, suggesting that calcium influx and patch formation enhance repair. In contrast, monomeric toxins were endocytosed. These data indicate that cells use two interrelated mechanisms of membrane repair: lipid-dependent MV shedding, which we term 'intrinsic repair', and patch formation by intracellular organelles. Endocytosis may act after membrane repair is complete by removing inactivated and monomeric toxins from the cell surface.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.