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

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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).