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Updated: May 12, 2026
10:07
High-throughput Measurement of Plasma Membrane Resealing Efficiency in Mammalian Cells
Published on: January 7, 2019
Ceramide in plasma membrane repair.
Annette Draeger1, Eduard B Babiychuk
1Department of Cell Biology, University of Bern, Bern, Switzerland. draeger@ana.unibe.ch
Handbook of Experimental Pharmacology
|April 9, 2013
Summary
Cells use ceramide to repair plasma membrane damage from toxins. Acid sphingomyelinase triggers inward repair, while neutral sphingomyelinase promotes outward toxin removal, ensuring cell survival.
Area of Science:
- Cell Biology
- Biochemistry
- Membrane Biology
Background:
- Pore-forming toxins perforate the plasma membrane, causing calcium influx and protein efflux.
- Cellular survival depends on identifying, plugging, and removing these membrane lesions.
Purpose of the Study:
- To elucidate the mechanisms by which cells repair plasma membrane damage induced by pore-forming toxins.
- To investigate the role of sphingomyelinases and ceramide in membrane repair pathways.
Main Methods:
- Studied Ca(2+)-driven lysosome fusion with the plasma membrane.
- Investigated the hydrolysis of sphingomyelin by acid and neutral sphingomyelinases.
- Proposed a model involving ceramide-induced membrane curvature for repair.
Main Results:
- Acid sphingomyelinase generates ceramide platforms, promoting inward vesiculation for endocytosis of damaged membrane.
- Neutral sphingomyelinase produces ceramide in the inner leaflet, inducing outward curvature to shed toxin-containing membrane.
- Annexin proteins act as Ca(2+) sensors and membrane fusion agents in this repair process.
Conclusions:
- Ceramide metabolism, regulated by distinct sphingomyelinases, dictates the directionality of membrane repair.
- Cellular repair mechanisms involve coordinated membrane trafficking and lipid remodeling.
- Annexin proteins are crucial mediators in toxin-induced membrane damage response.
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