Inhibition of DNA methylation is involved in transdifferentiation of myoblasts into smooth muscle cells.
Despite the importance of cell fate decisions regulated by epigenetic programming, no experimental model has been available to study transdifferentiation from myoblasts to smooth muscle cells. In the present study, we show that myoblast cells can be induced to transdifferentiate into smooth muscle cells by modulating their epigenetic programming. The DNA methylation inhibitor, zebularine, induced the morphological transformation of C2C12 myoblasts into smooth muscle cells accompanied by de novo synthesis of smooth muscle markers such as smooth muscle alpha-actin and transgelin. Furthermore, an increase of p21 and decrease of cyclinD1 mRNA were observed following zebularine treatment, pointing to inhibition of cell cycle progression. This system may provide a useful model for studying the early stages of smooth muscle cell differentiation.
Lee
Won Jun
WJ
College of Health Science, Ewha Womans University, Seoul 120-750, Korea.
Kim
Hye Jin
HJ
D000818:Animals; D054338:Cell Transdifferentiation / Q000502:physiology*; D002478:Cells, Cultured; D019938:Cyclin D1 / Q000096:biosynthesis; D003562:Cytidine / Q000031:analogs & derivatives / Q000494:pharmacology; D019175:DNA Methylation; D004790:Enzyme Induction; D044127:Epigenesis, Genetic; D051379:Mice; D009130:Muscle, Smooth / Q000166:cytology*; D032446:Myoblasts / Q000166:cytology* / Q000187:drug effects; D054462:p21-Activated Kinases / Q000096:biosynthesis
D019938:Cyclin D1; D003562:Cytidine; C009131:pyrimidin-2-one beta-ribofuranoside; D054462:p21-Activated Kinases