El Husseini Nazem, Schlisser Ava E, Hales Barbara F
*Department of Pharmacology and Therapeutics, McGill University, Montreal, Quebec, H3G 1Y6, Canada.
*Department of Pharmacology and Therapeutics, McGill University, Montreal, Quebec, H3G 1Y6, Canada
Toxicol Sci. 2016 Aug;152(2):297-308. doi: 10.1093/toxsci/kfw089. Epub 2016 May 13.
Hydroxyurea, an anticancer agent and potent teratogen, induces oxidative stress and activates a DNA damage response pathway in the gestation day (GD) 9 mouse embryo. To delineate the stress response pathways activated by this drug, we investigated the effect of hydroxyurea exposure on the transcriptome of GD 9 embryos. Timed pregnant CD-1 mice were treated with saline or hydroxyurea (400 mg/kg or 600 mg/kg) on GD 9; embryonic gene and protein expression were examined 3 h later. Microarray analysis revealed that the expression of 1346 probe sets changed significantly in embryos exposed to hydroxyurea compared with controls; the P53 signaling pathway was highly affected. In addition, P53 related family members, P63 and P73, were predicted to be activated and had common and unique downstream targets. Western blot analysis revealed that active phospho-P53 was significantly increased in drug-exposed embryos; confocal microscopy showed that the translocation of phospho-P53 to the nucleus was widespread in the embryo. Furthermore, qRT-PCR showed that the expression of P53-regulated genes (Cdkn1A, Fas, and Trp53inp1) was significantly upregulated in hydroxyurea-exposed embryos; the concentration of the redox sensitive P53INP1 protein was also increased in a hydroxyurea dose-dependent fashion. Thus, hydroxyurea elicits a significant effect on the transcriptome of the organogenesis stage murine embryo, activating several key developmental signaling pathways related to DNA damage and oxidative stress. We propose that the P53 pathway plays a central role in the embryonic stress response and the developmental outcome after teratogen exposure.
羟基脲是一种抗癌药物和强效致畸剂,可诱导氧化应激并激活妊娠第9天(GD9)小鼠胚胎中的DNA损伤反应途径。为了阐明这种药物激活的应激反应途径,我们研究了羟基脲暴露对GD9胚胎转录组的影响。在GD9对定时怀孕的CD-1小鼠用生理盐水或羟基脲(400mg/kg或600mg/kg)进行处理;3小时后检测胚胎基因和蛋白质表达。微阵列分析显示,与对照组相比,暴露于羟基脲的胚胎中1346个探针集的表达发生了显著变化;P53信号通路受到高度影响。此外,预测P53相关家族成员P63和P73被激活,并且具有共同和独特的下游靶点。蛋白质印迹分析显示,药物暴露胚胎中活性磷酸化P53显著增加;共聚焦显微镜显示,磷酸化P53向细胞核的易位在胚胎中广泛存在。此外,qRT-PCR显示,在暴露于羟基脲的胚胎中,P53调节基因(Cdkn1A、Fas和Trp53inp1)的表达显著上调;氧化还原敏感的P53INP1蛋白的浓度也以羟基脲剂量依赖性方式增加。因此,羟基脲对器官发生阶段小鼠胚胎的转录组产生显著影响,激活了与DNA损伤和氧化应激相关的几个关键发育信号通路。我们提出,P53途径在胚胎应激反应和致畸剂暴露后的发育结果中起核心作用。