Inhibition of NADH/NADPH oxidase affects signal transduction by growth factor receptors in normal fibroblasts
Inhibition of NADH/NADPH oxidase affects signal transduction by growth factor receptors in normal fibroblasts
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DOI：
10.1006/abbi.2001.2641
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发表时间：
2002-01-15
影响因子：
3.9
通讯作者：
Cimino, F
中科院分区：
文献类型：
--
作者：
Ammendola, R;Ruocchio, MR;Cimino, F
活性氧在有丝分裂信号转导中可能是第二信使。我们证明，在正常的成纤维细胞的治疗与两个抑制剂的吞噬NADH/NADPH氧化酶防止血小板衍生的生长因子受体的酪氨酸磷酸化后，暴露的血清剥夺细胞的生长因子。此外，NADH/NADPH氧化酶的抑制消除了细胞暴露于生长因子时发生的ERK活化和p21（waf 1）积累。最后，NADH/NADPH抑制剂阻止由血清和由佛波醇12-肉豆蔻酸酯-13-乙酸酯诱导的p66（Shc）Ser-磷酸化，这表明活性氧物质的直接靶标位于连接生长因子受体与Ras的机制的上游。(C)2002年，Elsevier Science。
Reactive oxygen species have been implicated as possible second messengers in mitogenic signal transduction. We demonstrate that in normal fibroblasts the treatment with the two inhibitors of phagocytic NADH/NADPH oxidase prevents tyrosine phosphorylation of platelet-derived growth factor receptor upon the exposure of serum-deprived cells to growth factors. Furthermore, the inhibition of NADH/NADPH oxidase abolishes ERKs activation and p21(waf1) accumulation that occurs when cells are exposed to growth factors. Finally, NADH/NADPH inhibitors prevent the p66(Shc) Ser-phosphorylation induced by serum and by phorbol 12-myristate-13-acetate, which suggests that the direct target(s) of reactive oxygen species is(are) located upstream from the machinery connecting growth factor receptors to Ras. (C) 2002 Elsevier Science.