Antisense c-myc oligonucleotide promotes chondrogenesis and enhances RA responsiveness of mouse limb mesenchymal cells in vitro.
To examine the role of c-myc protein during chondrogenesis, we exposed 11 day p.c. mouse limb mesenchymal cells to the antisense c-myc oligonucleotide in micromass culture. The antisense oligonucleotide inhibited the c-myc protein expression, and intensely promoted chondrogenesis in the exposed cells. Most of the cells differentiated into cartilaginous cells, whereas they differentiated into cartilaginous and fibrous cells under the control conditions. The antisense oligonucleotide increased the inhibitory efficiency of all-trans retinoic acid (RA) to the chondrogenesis. These results suggest that the c-myc protein suppress the chondrogenesis and reduces RA responsiveness in the limb mesenchymal cells.
Motoyama
J
J
Department of Developmental Biology, Graduate School of Dentistry, Tokyo Medical and Dental University, Japan.
Eto
K
K
D000818:Animals; D001483:Base Sequence; D002356:Cartilage / Q000196:embryology*; D002454:Cell Differentiation; D046508:Culture Techniques; D008648:Mesoderm / Q000166:cytology; D051379:Mice; D008810:Mice, Inbred C57BL; D008969:Molecular Sequence Data; D016376:Oligonucleotides, Antisense / Q000494:pharmacology; D016271:Proto-Oncogene Proteins c-myc / Q000037:antagonists & inhibitors / Q000235:genetics / Q000502:physiology*; D014212:Tretinoin / Q000494:pharmacology*
D016376:Oligonucleotides, Antisense; D016271:Proto-Oncogene Proteins c-myc; D014212:Tretinoin