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Updated: Jan 24, 2026

Imaging FITC-dextran as a Reporter for Regulated Exocytosis
Published on: June 20, 2018
Arachidonic acid and lysophosphatidylcholine inhibit multiple late steps of regulated exocytosis
Deepti Dabral1, Jens R Coorssen2
1Molecular Physiology, Molecular Medicine Research Group, School of Medicine, Western Sydney University, Campbelltown Campus, NSW, 2560, Australia.
Abstract:
The canonical Phospholipase A2 (PLA2) metabolites lysophosphatidylcholine (LPC) and arachidonic acid (ARA) affect regulated exocytosis in a wide variety of cells and are proposed to directly influence membrane merger owing to their respective spontaneous curvatures. According to the Stalk-pore hypothesis, negative curvature ARA inhibits and promotes bilayer merger upon introduction into the distal or proximal monolayers, respectively; in contrast, with positive curvature, LPC has the opposite effects. Using fully primed, release-ready native cortical secretory vesicles (CV), well-established fusion assays and standardized lipid analyses, we show that exogenous ARA and LPC, as well as their non-metabolizable analogous, ETYA and ET-18-OCH3, inhibit the docking/priming and membrane merger steps, respectively, of regulated exocytosis.
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