RETINOIC ACID TREATMENT INDUCES CELL-DEATH AND THE PROTEIN EXPRESSIONOF RETINOIC ACID RECEPTOR-BETA IN THE MESENCHYMAL CELLS OF MOUSE FACIAL PRIMORDIA IN-VITRO

We isolated mesenchymal cells from individual facial primordia of mous e embryos on 11 days post coitum and examined the effects of retinoic acid (RA) on chondrogenesis, induction of cell death, and the protein expression of retinoic acid receptor (RAR) beta and gamma in micromass culture. Under the control condition, cells of both medial and latera l nasal prominences (MNP and LNP) displayed high chondrogenic potentia l, while those of maxillary and mandibular prominences (Mx and Md) had constant growth activity and low chondrogenic potential. Though none of the cells expressed detectable levels of the RAR beta protein, RAR gamma was expressed in the cells of all the facial primordia. One mu M RA inhibited the chondrogenesis, and induced cell death accompanied w ith the induction of the RAR beta protein in LNP, Mx and Md cells with in 6 hr. On the contrary, both cell death and RAR beta protein inducti on were detected in the MNP cells treated with RA for 24 hr. These res ults suggest that the RAR beta is involved in the process of the cell death induced by the RA treatment in the mesenchymal cells of the mous e facial primordia.