Figure 4. TGF-β1 leads to an increase of 1,25D3-responsive genes in wounds by activation of CYP27B1.
Keratinocytes were pretreated with the VDR antagonist ZK159222 (VAZ; 10–7 M) or the CYP27B1 antagonist itraconazole (ITRA; 10–7 M) and then stimulated with TGF-β1 (1 ng/ml) in the presence or absence of 25D3 (10 nM) for 24 hours. Expression of cathelicidin (A), CD14 (B), and TLR2 (C) mRNA was determined as described in Figure 2. Induction of these innate immune effector and response genes by TGF-β1 found in wounds was dependent on the availability of 25D3 and the activity of CYP27B1 or a functional VDR. Data are mean ± SD of a single experiment performed in triplicate and are representative of 3 independent experiments. *P < 0.05, **P < 0.01, Student’s t test.