| First Author | Tamura Y | Year | 2011 |
| Journal | FEBS Lett | Volume | 585 |
| Issue | 19 | Pages | 3058-64 |
| PubMed ID | 21888904 | Mgi Jnum | J:176425 |
| Mgi Id | MGI:5291842 | Doi | 10.1016/j.febslet.2011.08.028 |
| Citation | Tamura Y, et al. (2011) NO donor induces Nec-1-inhibitable, but RIP1-independent, necrotic cell death in pancreatic beta-cells. FEBS Lett 585(19):3058-64 |
| abstractText | Nitric oxide (NO) has been implicated in pancreatic beta-cell death in the development of diabetes. The mechanisms underlying NO-induced beta-cell death have not been clearly defined. Recently, receptor-interacting protein-1 (RIP1)-dependent necrosis, which is inhibited by necrostatin-1, an inhibitor of RIP1, has emerged as a form of regulated necrosis. Here, we show that NO donor-induced beta-cell death was inhibited by necrostatin-1. Unexpectedly, however, RIP1 knockdown neither inhibited cell death nor altered the protective effects of necrostatin-1 in NO donor-treated beta-cells. These results indicate that NO donor induces necrostatin-1-inhibitable necrotic beta-cell death independent of RIP1. Our findings raise the possibility that NO-mediated beta-cell necrosis may be a novel form of signal-regulated necrosis, which play a role in the progression of diabetes. |
