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NO donor induces Nec-1-inhibitable, but RIP1-independent, necrotic cell death in pancreatic ?-cells.

ABSTRACT: Nitric oxide (NO) has been implicated in pancreatic ?-cell death in the development of diabetes. The mechanisms underlying NO-induced ?-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 ?-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 ?-cells. These results indicate that NO donor induces necrostatin-1-inhibitable necrotic ?-cell death independent of RIP1. Our findings raise the possibility that NO-mediated ?-cell necrosis may be a novel form of signal-regulated necrosis, which play a role in the progression of diabetes.

SUBMITTER: Tamura Y 

PROVIDER: S-EPMC3304503 | biostudies-literature | 2011 Oct

REPOSITORIES: biostudies-literature

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NO donor induces Nec-1-inhibitable, but RIP1-independent, necrotic cell death in pancreatic β-cells.

Tamura Yoshiaki Y   Chiba Yuko Y   Tanioka Toshihiro T   Shimizu Nobuyuki N   Shinozaki Shohei S   Yamada Marina M   Kaneki Kentaro K   Mori Seijiro S   Araki Atsushi A   Ito Hideki H   Kaneki Masao M  

FEBS letters 20110828 19

Nitric oxide (NO) has been implicated in pancreatic β-cell death in the development of diabetes. The mechanisms underlying NO-induced β-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 β-cell death was inhibited by necrostatin-1. Unexpectedly, however, RIP1 knockdown neither inhibited cell death no  ...[more]

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