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• W1992459513 abstract "The function of P2X7 receptors (ATP-gated ion channels) in innate immune cells is unclear. In the setting of Toll-like receptor (TLR) stimulation, secondary activation of P2X7 ion channels has been linked to pro-caspase-1 cleavage and cell death. Here we show that cell death is a surprisingly early triggered event. We show using live-cell imaging that transient (1–4 min) stimulation of mouse macrophages with high extracellular ATP ([ATP]e) triggers delayed (hours) cell death, indexed as DEVDase (caspase-3 and caspase-7) activity. Continuous or transient high [ATP]e did not induce cell death in P2X7-deficient (P2X7−/−) macrophages or neutrophils (in which P2X7 could not be detected). Blocking sustained Ca2+ influx, a signature of P2X7 ligation, was highly protective, whereas no protection was conferred in macrophages lacking caspase-1 or TLR2 and TLR4. Furthermore, pannexin-1 (Panx1) deficiency had no effect on transient ATP-induced delayed cell death or ATP-induced Yo-Pro-1 uptake (an index of large pore pathway formation). Thus, “transient” P2X7 receptor activation and Ca2+ overload act as a death trigger for native mouse macrophages independent of Panx1 and pro-inflammatory caspase-1 and TLR signaling. The function of P2X7 receptors (ATP-gated ion channels) in innate immune cells is unclear. In the setting of Toll-like receptor (TLR) stimulation, secondary activation of P2X7 ion channels has been linked to pro-caspase-1 cleavage and cell death. Here we show that cell death is a surprisingly early triggered event. We show using live-cell imaging that transient (1–4 min) stimulation of mouse macrophages with high extracellular ATP ([ATP]e) triggers delayed (hours) cell death, indexed as DEVDase (caspase-3 and caspase-7) activity. Continuous or transient high [ATP]e did not induce cell death in P2X7-deficient (P2X7−/−) macrophages or neutrophils (in which P2X7 could not be detected). Blocking sustained Ca2+ influx, a signature of P2X7 ligation, was highly protective, whereas no protection was conferred in macrophages lacking caspase-1 or TLR2 and TLR4. Furthermore, pannexin-1 (Panx1) deficiency had no effect on transient ATP-induced delayed cell death or ATP-induced Yo-Pro-1 uptake (an index of large pore pathway formation). Thus, “transient” P2X7 receptor activation and Ca2+ overload act as a death trigger for native mouse macrophages independent of Panx1 and pro-inflammatory caspase-1 and TLR signaling." @default.
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• W1992459513 date "2012-03-01" @default.
• W1992459513 modified "2023-09-26" @default.
• W1992459513 title "Transient P2X7 Receptor Activation Triggers Macrophage Death Independent of Toll-like Receptors 2 and 4, Caspase-1, and Pannexin-1 Proteins" @default.
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• W1992459513 doi "https://doi.org/10.1074/jbc.m111.332676" @default.
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