INTERLEUKIN-1 BETA-INDUCED NITRIC-OXIDE PRODUCTION ACTIVATES APOPTOSIS IN PANCREATIC RINM5F CELLS
INTERLEUKIN-1 BETA-INDUCED NITRIC-OXIDE PRODUCTION ACTIVATES APOPTOSIS IN PANCREATIC RINM5F CELLS
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DOI：
10.1006/excr.1994.1187
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发表时间：
1994-07-01
影响因子：
3.7
通讯作者：
NICOTERA, P
中科院分区：
文献类型：
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作者：
ANKARCRONA, M;DYPBUKT, JM;NICOTERA, P
I 型胰岛素依赖性糖尿病期间细胞因子的产生与β细胞功能的改变有关，例如抑制葡萄糖刺激的胰岛素分泌。包括白细胞介素 1 β (IL-1 β) 在内的细胞因子的这种副作用和其他副作用涉及诱导一氧化氮合酶并产生一氧化氮。在这里，我们证明 IL-1 beta 会诱导胰腺 β 细胞系 RINm5F 细胞凋亡。用IL-1β处理的细胞经历DNA断裂、核浓缩和凋亡体形成。一氧化氮的产生先于细胞凋亡的这些典型特征的出现。 N-G-单甲基-L-精氨酸抑制一氧化氮合酶活性可阻止 IL-1 β 诱导的一氧化氮生成和凋亡细胞杀伤。这些结果表明，除了已知的 β 细胞功能改变外，IL-1 β 诱导的一氧化氮生成还可激活细胞死亡程序。 1994 学术出版社
Cytokine production during type I insulin-dependent diabetes mellitus has been linked to alterations in beta-cell function such as inhibition of glucose-stimulated insulin secretion. This and other adverse effects of cytokines, including interleukin-1 beta (IL-1 beta) involve the induction of nitric oxide synthase, with production of nitric oxide. Here, we show that IL-1 beta induces apoptosis in a pancreatic beta-cell line, RINm5F cells. Cells treated with IL-1 beta underwent DNA fragmentation, nuclear condensation, and apoptotic body formation. The production of nitric oxide preceded the appearance of these typical features of apoptosis. Inhibition of the nitric oxide synthase activity by N-G-monomethyl-L-arginine prevented IL-1 beta-induced nitric oxide generation and apoptotic cell killing. These results show that-besides the known alterations in beta-cell function-IL-1 beta-induced nitric oxide production activates the cell death program. 1994 Academic Press, Inc.