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Expression of the P2X7 Receptor Increases the Ca2+ Content of the Endoplasmic Reticulum, Activates NFATc1, and Protects from Apoptosis*

By Elena Adinolfi, Maria Giulia Callegari, Maria Cirillo, Paolo Pinton, Carlotta Giorgi, Dario Cavagna, Rosario Rizzuto and Francesco Di Virgilio


The P2X7 receptor is known for the cytotoxic activity because of its ability to cause opening of non-selective pores in the plasma membrane and activate apoptotic caspases. A key factor of P2X7-dependent cytotoxicity is the massive intracellular Ca2+ increase triggered by its activation. Here we show that P2X7 transfection increased the ability of the endoplasmic reticulum to accumulate, store, and release Ca2+. This caused a larger agonist-stimulated increase in cytosol and mitochondrial Ca2+ in P2X7 transfectants than in mock transfected cells. P2X7 transfectants survived and even proliferated in serum-free conditions and were resistant to apoptosis triggered by ceramide, staurosporin, or intracellular Zn2+ chelation. Finally, the nuclear factor of activated T cells complex 1 (NFATc1) was strongly activated in the P2X7 transfectants. These observations support our previous finding that the P2X7 receptor under tonic conditions of stimulation, i.e. those observed in response to basal ATP release, has an anti-apoptotic or even growth promoting rather than cytotoxic activity

Topics: Mechanisms of Signal Transduction
Publisher: American Society for Biochemistry and Molecular Biology
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Provided by: PubMed Central
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