Abstract
Resealing allows cells to mend damaged membranes rapidly when plasma membrane (PM) disruptions occur. Models of PM repair mechanisms include the "lipid-patch", "endocytic removal", and "macro-vesicle shedding" models, all of which postulate a dependence on local increases in intracellular Ca(2+) at injury sites. Multiple calcium sensors, including synaptotagmin (Syt) VII, dysferlin, and apoptosis-linked gene-2 (ALG-2), are involved in PM resealing, suggesting that Ca(2+) may regulate multiple steps of the repair process. Although earlier studies focused exclusively on external Ca(2+), recent studies suggest that Ca(2+) release from intracellular stores may also be important for PM resealing. Hence, depending on injury size and the type of injury, multiple sources of Ca(2+) may be recruited to trigger and orchestrate repair processes. In this review, we discuss the mechanisms by which the resealing process is promoted by vesicular Ca(2+) channels and Ca(2+) sensors that accumulate at damage sites.