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Arachidonic acid and lysophosphatidylcholine inhibit multiple late steps of regulated exocytosis
- Dabral, Deepti, Coorssen, Jens R.
- Biochemical and biophysical research communications 2019 v.515 no.2 pp. 261-267
- arachidonic acid, exocytosis, lysophosphatidylcholine, metabolites, phospholipase A2, secretory granules
- 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.