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Updated: May 7, 2026

Live Imaging Assay for Assessing the Roles of Ca2+ and Sphingomyelinase in the Repair of Pore-forming Toxin Wounds
Published on: August 25, 2013
Caveolae internalization repairs wounded cells and muscle fibers
Matthias Corrotte1, Patricia E Almeida, Christina Tam
1Department of Cell Biology and Molecular Genetics , University of Maryland , College Park , United States.
Cell membrane repair involves calcium-triggered lysosome release and lesion removal by caveolar endocytosis. This process is crucial for maintaining muscle fiber integrity and preventing muscular dystrophy.
Area of Science:
- Cell Biology
- Membrane Biology
- Muscle Physiology
Background:
- Plasma membrane wound repair is essential for cell survival.
- Defective sarcolemma resealing in muscle fibers leads to muscular dystrophy.
- Caveolae, caveolin, and cavin proteins are implicated in muscle pathology, but the mechanism is unclear.
Purpose of the Study:
- To elucidate the mechanism of plasma membrane wound repair.
- To investigate the role of caveolae in membrane repair and muscle integrity.
- To explain the muscle pathology associated with mutations in caveolae proteins.
Main Methods:
- Studied Ca(2+)-triggered exocytosis of lysosomes.
- Investigated the release of acid sphingomyelinase.
- Analyzed lesion removal by caveolar endocytosis using toxin SLO and caveolin depletion.
Main Results:
- Membrane wounding triggers Ca(2+)-dependent lysosome exocytosis and acid sphingomyelinase release.
- Caveolar endocytosis mediates rapid removal of membrane lesions.
- Depletion of caveolin impairs plasma membrane resealing and promotes toxin entry via caveolar vesicles.
Conclusions:
- Caveolar endocytosis is a key mechanism for removing membrane lesions and maintaining plasma membrane integrity.
- This pathway is critical for muscle fiber integrity, and its dysfunction explains muscular dystrophy linked to caveolae protein mutations.
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