Wlodraczyk B, Bennett G D, Calvin J A, Craig J C, Finnell R H
Department of Veterinary Anatomy and Public Health, Texas A & M University, College Station 77843-4458, USA.
Dev Genet. 1996;18(4):306-15. doi: 10.1002/(SICI)1520-6408(1996)18:4<306::AID-DVG4>3.0.CO;2-D.
We examined the morphological and molecular consequences of acute in utero exposure to teratogenic concentrations of arsenate. The treatment produced a dose-related increase in neural tube defects, along with a significant alteration in the pattern of gene expression for several transcription factors (creb, Hox 3.1, Pax3, and Emx-1) that were examined using in situ transcription and antisense RNA amplification procedures. On gestational day 9:0, there was a significant delay in the embryos progression through neural tube closure, accompanied by a significant downregulation of Hox 3.1 expression and a significant upregulation of Pax3, Emx-1, and creb. As both Hox 3.1 and Pax3 serve to regulate N-CAM expression, it is possible that abnormalities associated with N-CAM may compromise neural crest cell migration and normal neural tube closure.
我们研究了子宫内急性暴露于致畸浓度砷酸盐的形态学和分子学后果。该处理导致神经管缺陷呈剂量相关增加，同时使用原位转录和反义RNA扩增程序检测的几种转录因子（creb、Hox 3.1、Pax3和Emx-1）的基因表达模式发生显著改变。在妊娠第9.0天，胚胎通过神经管闭合的进程显著延迟，同时伴有Hox 3.1表达的显著下调以及Pax3、Emx-1和creb的显著上调。由于Hox 3.1和Pax3都用于调节N-CAM表达，与N-CAM相关的异常可能会损害神经嵴细胞迁移和正常神经管闭合。
