P2X7-induced apoptosis decreases by aging in mice myeloblasts

• Published in: Experimental gerontology Vol. 42; no. 4; pp. 320 - 326
• Main Authors: Paredes-Gamero, Edgar Julian, Dreyfuss, Juliana Luporini, Nader, Helena B, Miyamoto Oshiro, Maria Etsuko, Ferreira, Alice Teixeira
• Format: Journal Article
• Language: English
• Published: England 01.04.2007
• Subjects: Adenosine Diphosphate - physiology; Adenosine Triphosphate - analogs & derivatives; Adenosine Triphosphate - pharmacology; Adenosine Triphosphate - physiology; Affinity Labels - pharmacology; Aging - physiology; Animals; Apoptosis - physiology; Granulocyte Precursor Cells - physiology; Hindlimb; Male; Mice; Mice, Inbred C57BL; Purinergic P2 Receptor Antagonists; Receptors, Purinergic P2 - physiology; Receptors, Purinergic P2X7; Uridine Triphosphate - physiology
• ISSN: 0531-5565
• DOI: 10.1016/j.exger.2006.11.011

In the current study, the ability of ATP to promote apoptosis in myeloblasts at different ages was investigated. We have observed that high concentration of extracellular ATP (>1mM), which activates P2X(7) receptor, produced cell shrinkage an increase in the number of events in the sub-G(0)/G(1) region of the cellular cycle and annexin-V/propidium iodide label, which characterizes the apoptotic cell death. In addition, BzATP produced apoptosis, but not ADP and UTP. Gr-1(+) cells express the P2X(7) receptor and oxidized ATP, a specific P2X(7) inhibitor, blocked the ATP-dependent apoptosis. ATP-dependent apoptosis is decreased by aging in myeloblasts of 12 and 22-month-old mice. Furthermore, P2X(7) expression decrease was observed in older mice, explaining apoptosis decrease. This decrease in apoptosis by aging may be related to some diseases in the myelocyte lineage.