Extracellular ATP as a trigger for apoptosis or programmed cell death.

• DOI: 10.1083/jcb.112.2.279
• Publication Date: 2004-05-15T00:18:20Z
• Authors: L M Zheng; A Zychlinsky; C C Liu; D M Ojcius; J D Young
• Keywords: Fragmentation; Apoptotic DNA fragmentation; Thymocyte

Extracellular ATP is shown here to induce programmed cell death (or apoptosis) in thymocytes and certain tumor lines. EM studies indicate that the ATP-induced of susceptible cells follows morphological changes usually associated with glucocorticoid-induced apoptosis thymocytes. These include condensation chromatin, blebbing surface, breakdown nucleus. Cytotoxicity assays using double-labeled show ATP-mediated lysis accompanied by fragmentation target DNA. DNA can be set off but not nonhydrolysable analogue gamma S nor other nucleoside-5'-triphosphates. 51Cr release blocked pretreated inhibitors protein or RNA synthesis endonuclease inhibitor, zinc; whereas pretreatment calmidazolium, a potent calmodulin antagonist, blocks both release. The biochemical caused are preceded rapid increase cytoplasmic calcium cell. Calcium fluxes themselves, however, sufficient cause apoptosis, as pore-forming protein, perforin, causes without apoptosis. Taken together, these results through two independent mechanisms, one which, requiring an active participation on part cell, takes place