ABSTRACT
Secretory defects in cells are responsible for a host of debilitating diseases. Since the mid 1950s, it was believed that during cell secretion, secretory vesicles completely merge at the cell plasma membrane, resulting in the diffusion of intravesicular contents to the cell exterior and the compensatory retrieval of the excess membrane by endocytosis. Porosomes are supramolecular lipoprotein structures at the cell plasma membrane, where membrane-bound secretory vesicles transiently dock and fuse to release intravesicular contents to the outside during cell secretion. As pancreatic acinar cells are slow secretory cells, they were ideal for investigation of the molecular steps involved in cell secretion. Calcium bridging of apposing bilayers may lead to the release of water from the hydrated Ca2+ ion, leading to bilayer destabilization and membrane fusion. Atomic force microscopy micrographs of the specific localization of gold-tagged amylase-specific antibodies at depressions, following stimulation of cell secretion, conclusively demonstrated depressions as the cellular secretory portal.
