Calcium uptake via endocytosis with rapid release from acidifying endosomes

• Published in: Current biology 1998-12, Vol.8 (24), p.1335-1338
• Main Authors: Gerasimenko, Julia V., Tepikin, Alexei V., Petersen, Ole H., Gerasimenko, Oleg V.
• Format: Article
• Language: English
• Subjects: 3T3 Cells; Animals; Anti-Bacterial Agents - pharmacology; Calcium - metabolism; Endocytosis - drug effects; Endocytosis - physiology; Endosomes - drug effects; Endosomes - metabolism; Enzyme Inhibitors - pharmacology; Fluorescent Dyes; Hydrogen-Ion Concentration; Ion Transport - drug effects; Kinetics; Macrolides; Mice; Microscopy, Confocal; Proton-Translocating ATPases - antagonists & inhibitors
• ISSN: 0960-9822; 1879-0445
• DOI: 10.1016/S0960-9822(07)00565-9

A number of specific cellular Ca2+ uptake pathways have been described in many different cell types [1–3].The possibility that substantial quantities of Ca2+ could be imported via endocytosis has essentially been ignored, although it has been recognized that endosomes can store Ca2+[4,5]. Exocrine cells can release significant amounts of Ca2+ via exocytosis [6], so we have investigated the fate of Ca2+ taken up via endocytosis into endosomes. Ca2+-sensitive and H+-sensitive fluorescent probes were placed in the extracellular solution and subsequently taken up into fibroblasts by endocytosis. Confocal microscopy was used to assess the distribution of fluorescence intensity. Ca2+ taken up by endocytosis was lost from the endosomes within a few minutes, over the same period as endosomal acidification took place. The acidification was inhibited by reducing the extracellular Ca2+ concentration, and Ca2+ loss from the endosomes was blocked by bafilomycin (100 nM), a specific inhibitor of the vacuolar proton ATPase. Quantitative evaluation indicated that endocytosis causes substantial import of Ca2+ because of rapid loss from early endosomes.