| First Author | Lépine S | Year | 2006 |
| Journal | Biochim Biophys Acta | Volume | 1761 |
| Issue | 1 | Pages | 73-82 |
| PubMed ID | 16325464 | Mgi Jnum | J:110330 |
| Mgi Id | MGI:3640029 | Doi | 10.1016/j.bbalip.2005.10.001 |
| Citation | Lepine S, et al. (2006) ATP-induced apoptosis of thymocytes is mediated by activation of P2 X 7 receptor and involves de novo ceramide synthesis and mitochondria. Biochim Biophys Acta 1761(1):73-82 |
| abstractText | Thymocytes were reported to undergo apoptosis in the presence of extracellular ATP through the activation of the purinergic receptors P2 X 1R, P2 X 7R or both. We investigated the identity of the P2 X R and the signaling pathways involved in ATP-mediated apoptosis. Apoptosis elicited by ATP was prevented by inhibition of P2 X 7R, or in thymocytes bearing a mutated P2 X 7R, and reproduced with a P2 X 7R agonist, but not with a P2 X 1R agonist. Stimulation of thymocytes with either ATP or a P2 X 7R agonist was found to stimulate a late de novo ceramide synthesis and mitochondrial alterations. Inhibition of either processes attenuated apoptosis. Interestingly, stimulation with either ATP or a P2 X 1R agonist induced an early ceramide accumulation and a weak caspases-3/7 activation that did not lead to apoptosis. In conclusion, de novo ceramide generation and mitochondrial alterations, both resulting from P2 X 7R activation, were implicated in ATP-induced thymocyte apoptosis. |
