Dealing with damage: Plasma membrane repair mechanisms

•Mechanical injuries within the plasma membrane are repaired by lysosomal exocytosis.•Toxin-induced membrane perforations are shed as microvesicles or endocytosed.•Plasmalemmal repair profits from destabilization of the submembranous cytoskeleton.•An increase in membrane surface reduces the likelihood of lethal injury.•Microvilli and ciliae serve as passive, membrane blebs as active toxin traps.

Eukaryotic cells have developed repair mechanisms, which allow them to reseal their membrane in order to prevent the efflux of cytoplasmic constituents and the uncontrolled influx of calcium. After injury, the Ca2+-concentration gradient fulfils a dual function: it provides guidance cues for the repair machinery and directly activates the molecules, which have a repair function. Depending on the nature of injury, the morphology of the cell and the severity of injury, the membrane resealing can be effected by lysosomal exocytosis, microvesicle shedding or a combination of both. Likewise, exocytosis is often followed by the endocytic uptake of lesions. Additionally, since plasmalemmal resealing must be attempted, even after extensive injury in order to prevent cell lysis, the restoration of membrane integrity can be achieved by ceramide-driven invagination of the lipid bilayer, during which the cell is prepared for apoptotic disposal. Plasmalemmal injury can be contained by a surfeit of plasma membrane, which serves as a trap for toxic substances: either passively by an abundance of cellular protrusions, or actively by membrane blebbing.