The resealing factor S100A11 interacts with annexins and extended synaptotagmin-1 in the course of plasma membrane wound repair.

After damage, cells repair their plasma membrane in an active process that is driven by Ca entering through the wound. This triggers a range of Ca-regulated events such as the translocation of different Ca-binding proteins to the wound site which likely function in the repair process. The translocated proteins include Ca/phospholipid binding proteins of the annexin (ANX) family and S100A11, an EF hand-type Ca-binding protein which can interact with ANX.

Plasma membrane wound repair is characterized by extensive membrane lipid and protein rearrangements in vascular endothelial cells.

Vascular endothelial cells are subject to mechanical stress resulting from blood flow and interactions with leukocytes. Stress occurs at the apical, vessel-facing cell surface and leads to membrane ruptures that have to be resealed to ensure cell survival. To mimic this process, we developed a laser ablation protocol selectively inducing wounds in the apical plasma membrane of endothelial cells.

Induction of Ca-Dependent Exocytotic Processes by Laser Ablation of Endothelial Cells.

Ca regulates a variety of cellular processes that are essential to maintain cell integrity and function. Different methods have been used to study these processes by increasing intracellular Ca levels. Here, we describe a protocol to initiate Ca-dependent membrane-related events, using laser ablation by near-infrared irradiation.

Annexins and plasma membrane repair.

Plasma membrane wound repair is a cell-autonomous process that is triggered by Ca 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.