Effect of triamcinolone acetonide on proliferation and collagen and glycosaminoglycan syntheses in palatal mesenchymal cells from the mouse fetus.

The present study was performed 1) to demonstrate the direct effects of triamcinolone acetonide (TA) at various concentrations on mouse fetal palatal mesenchyme (MFPM) cells with special reference to proliferating activity and collagen and glycosaminoglycan syntheses, and 2) to determine whether the effects of TA were glucocorticoid (GC) receptor-mediated. A low concentration of TA (10(-10) M) stimulated proliferating activity and hyaluronic acid (HA) synthesis. As TA concentrations were increased, proliferating activity and collagen synthesis were suppressed in a concentration-dependent manner, with especially marked suppression occurring at 10(-7) -10(-5) M. Rather mild reductions were observed in the rates of HA and total cellular protein synthesis. Further, it was demonstrated that MFPM cells have a single population of specific, high-affinity, saturable GC receptors which have an apparent dissociation constant (Kd) of 17 nM; and there are 24.2 X 10(4) binding sites per cell. Moreover, antagonistic effects of progesterone were observed on proliferating activity and collagen synthesis, suggesting that the responses of the cells to GC are receptor-mediated. The results show that MFPM cells are capable of responding to both physiological and pharmacological levels of GC directly, suggesting that either endogenous or exogenous high levels of GC may have the potential to interfere with mouse palate formation by perturbing the proliferating activity and synthesis of macromolecules in palatal mesenchymal cells.