Studies on molecular mechanisms of thalidomide-induced teratogenesis using human mesenchymal tem cells

沙利度胺致畸性的作用机制有很多，包括抑制血管生成或氧化性DNA损伤。我们对沙利度胺处理的人间充质干细胞和小鼠间充质干细胞样细胞进行了基因表达谱芯片分析。在人细胞中未观察到基因表达（包括氧化应激）的明显变化（10μM沙利度胺）。另一方面，在小鼠间充质干细胞样细胞（10-300μM沙利度胺）中观察到长非编码RNA的剂量依赖性减少。

There are many proposed mechanisms of action in thalidomide teratogenicity including inhibition of angiogenesis or oxidative DNA damage. We have undertaken a microarray gene expression analysis on human mesenchymal stem cells and mouse mesenchymal stem like cells treated with thalidomide. No clear changes of gene expression including oxidative stress were observed (10μM thalidomide) in the human cells. On the other hand, dose-dependent decrease of a long non-coding RNA was observed in mouse mesenchymal stem like cells (10-300μM thalidomide).