Plasma membrane wound repair is a cell-autonomous process that is triggered by Ca2+ entering through the site of injury and involves membrane resealing, i.e., re-establishment of a continuous plasma membrane, as well as remodeling of the cortical actin cytoskeleton. Among other things, the injury-induced Ca2+ elevation initiates the wound site recruitment of Ca2+-regulated proteins that function in the course of repair. Annexins are a class of such Ca2+-regulated proteins. They associate with acidic phospholipids of cellular membranes in their Ca2+ bound conformation with Ca2+ sensitivities ranging from the low to high micromolar range depending on the respective annexin protein. Annexins accumulate at sites of plasma membrane injury in a temporally controlled manner and are thought to function by controlling membrane rearrangements at the wound site, most likely in conjunction with other repair proteins such as dysferlin. Their role in membrane repair, which has been evidenced in several model systems, will be discussed in this chapter.
Keywords: Actin cytoskeleton; Calcium signaling; Endocytosis; Exocytosis; Membrane trafficking.
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