TABLE 4.
STAT1 and STAT3 account for PPARα or PPARβ/δ-mediated stimulation of hBD2 and hBD3 mRNA expression in human KC
| Treatmenta | Relative mRNA expression vs vehicle controlb |
|
|---|---|---|
| hBD2 | hBD3 | |
| Vehicle | 1.0 ± 0.1 | 1.0 ± 0.0 |
| Fludarabine | 0.4 ± 0.1 | 2.1 ± 0.3 |
| STA-21 | 0.5 ± 0.2 | 1.7 ± 0.2 |
| PPARα agonist | 4.1 ± 0.3* | 30.1 ± 6.4* |
| PPARα + fludarabine | 1.9 ± 0.3# | 13.1 ± 1.5# |
| PPARα + STA-21 | 1.2 ± 0.5# | 14.4 ± 3.3# |
| PPARβ/δ agonist | 5.2 ± 0.6* | 103.9 ± 13.1* |
| PPARβ/δ + fludarabine | 0.8 ± 0.4# | 38.1 ± 4.5# |
| PPARβ/δ + STA-21 | 0.9 ± 0.0# | 11.7 ± 1.9# |
a
Normal human KC were pretreated with an inhibitor of STAT1 (fludarabine [10 μM]) or STAT3 (STA-21 [2 μM]) for 30 min and then were incubated with or without a PPARα agonist (GW9578 [5 μM]) or PPARβ/δ agonist (GSK0742 [5 μM]) for 24 h.
b
Values are means ± SD (n = 3). *, P < 0.01 versus vehicle control; #, P < 0.01 versus each agonist alone.