Suppression of Gadd45 alleviates the G2/M blockage and the enhanced phosphorylation of p53 and p38 in zinc supplemented normal human bronchial epithelial cells
Suppression of Gadd45 alleviates the G2/M blockage and the enhanced phosphorylation of p53 and p38 in zinc supplemented normal human bronchial epithelial cells
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DOI：
10.3181/0708-rm-220
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发表时间：
2008-03-01
影响因子：
3.2
通讯作者：
Lei, Kai Y.
中科院分区：
文献类型：
--
作者：
Shih, Rita S. M.;Wong, Stephen H. K.;Lei, Kai Y.
充足的锌对最佳的细胞功能和生长至关重要。然而，过量的锌补充剂可能具有细胞毒性，并可能损害细胞生长。Gadd45作为细胞应激传感器在调节细胞对应激的信号转导中起着至关重要的作用。本研究旨在确定锌状态对缺锌和补锌的正常人支气管上皮细胞（NHBE）中Gadd45表达和细胞周期进展的影响，并揭示抑制Gadd45表达对该细胞类型细胞生长和细胞周期进展的分子机制。细胞在不同浓度的锌中培养1代；
An adequate zinc status is essential for optimal cellular functions and growth. Yet, excessive zinc supplementation can be cytotoxic and can impair cell growth. Gadd45 plays a vital role as cellular stress sensor in the modulation of cell signal transduction in response to stress. The present study was designed to determine the influence of zinc status on Gadd45 expression and cell cycle progression in zinc deficient and supplemented normal human bronchial epithelial (NHBE) cells, and to decipher the molecular mechanism(s) exerted by the suppression of Gadd45 expression on cell growth and cell cycle progression in this cell type. Cells were cultured for one passage in different concentration of zinc: