One class of molecules important in development and homeostasis is the vitamin A metabolites, including retinoic acid (RA) (reviewed in Underhill et al 1995). In the developing mammalian limb, RA affects the differentiation of many cell lineages, including those of mesenchymal origin. Administration of high doses of RA to mouse embryos in utero results in a wide range of birth defects that affect development of the limbs as well as other tissues (Kochhar 1973). The timing of RA treatment and the resultant limb defects appear to coincide with the timing of mesenchyme condensation and differentiation into chondrocytes. Further analysis has shown that RA inhibits chondrogenesis and it is most likely this activity that contributes to the aforementioned limb defects (Underhill & Weston 1998). Together, these results suggest that RA is a potent inhibitor of chondrogenesis.
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