A Nonsecosteroidal Vitamin D Receptor Modulator Ameliorates Experimental Autoimmune Encephalomyelitis without Causing Hypercalcemia
Figure 3
Compound A is less potent and efficacious in inducing the expression of vitamin D-responsive genes in intestinal cells. (a) Compound A shows weak potency in inducing the expression of endogenous CaT1 gene in differentiated Caco-2 cells. Taqman Q-PCR was performed on total RNA prepared from differentiated Caco-2 cells treated with various concentrations of 1,25-(OH)2D3 or compound A for 24 hours. Levels of GAPDH mRNA were measured in all the samples, and the results were normalized and presented (±SE) as relative light units (RLU) after normalization with the GAPDH transcript levels. (b) Compound A is a poor inducer of endogenous vitamin D-responsive genes in differentiated Caco-2 and rat duodenal cells. Taqman Q-PCR was performed on total RNA prepared from Caco-2 and rat duodenal IEC-6 cells treated with vehicle or 100 nM each of 1,25-(OH)2D3 or compound A for 24 hours. The fold induction of CYP24 and calbindin-9k transcripts relative to GAPDH transcripts is shown as mean ± SE of quadruplicate experiments.
