SPLENIC B-LYMPHOCYTE PROGRAMMED CELL-DEATH IS PREVENTED BY NITRIC-OXIDE RELEASE THROUGH MECHANISMS INVOLVING SUSTAINED BCL-2 LEVELS
SPLENIC B-LYMPHOCYTE PROGRAMMED CELL-DEATH IS PREVENTED BY NITRIC-OXIDE RELEASE THROUGH MECHANISMS INVOLVING SUSTAINED BCL-2 LEVELS
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DOI：
10.1172/jci117869
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发表时间：
1995-04-01
影响因子：
15.9
通讯作者：
BOSCA, L
中科院分区：
文献类型：
--
作者：
GENARO, AM;HORTELANO, S;BOSCA, L
在一氧化氮或一氧化氮供体物质存在的情况下孵育离体培养的成熟 B 细胞可延迟程序性细胞死亡，这一点可通过琼脂糖凝胶电泳中 DNA 阶梯的出现或通过 DNA 的流式细胞术分析来确定。一氧化氮还可以将 B 细胞从抗原诱导的细胞凋亡中拯救出来，但无法提供将抗原引发的信号转化为增殖反应的共刺激信号。一氧化氮对程序性细胞死亡的保护作用可以通过用环状 GMP 的渗透类似物处理细胞来重现。关于一氧化氮防止 B 细胞凋亡的机制，我们观察到一氧化氮的释放可以防止原癌基因 bcl-2 在 mRNA 和蛋白质水平上的表达下降，表明存在将一氧化氮信号传导与 Bcl-2 表达联系起来的未知途径。
Incubation of ex vivo cultured mature B cells in the presence of nitric oxide or nitric oxide-donor substances delays programmed cell death as determined by the appearance of DNA laddering in agarose gel electrophoresis or by flowcytometry analysis of DNA. Nitric oxide also rescues B cells from antigen-induced apoptosis but fails to provide a co-stimulatory signal that converts the signal elicited by the antigen into a proliferative response, The protective effects of nitric oxide against programmed cell death can be reproduced by treatment of the cells with permeant analogues of cyclic GMP. Regarding the mechanisms by which nitric oxide prevents apoptosis in B cells, we have observed that nitric oxide release prevents the drop in the expression of the protooncogene bcl-2, both at the mRNA and protein levels, suggesting the existence of an unknown pathway that links nitric oxide signaling with Bcl-2 expression.