Inhibition as a Novel Therapeutic Target for Keloid Disease.

Inactivation of poly(ADP-ribose) polymerase 1 () has been found to have protective effect in several fibrotic diseases. But the effect is not studied yet in keloids. Herein, we evaluated the therapeutic effect of inhibitor, rucaparib, for keloids. The protein expressions of and smad3 were evaluated with western blotting in keloids and controls. The effect of rucaparib was evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and migration assay. We further analyzed the effect of rucaparib on patient-derived keloid xenograft murine model. The protein expressions of and smad3 were significantly higher in keloid tissue. Rucaparib (20 μM) significantly suppressed the proliferation of keloid fibroblasts. Moreover, the combination of rucaparib (20 μM) and triamcinolone (50 μM) showed additive suppressive effect on keloid fibroblasts. Migration assay showed that rucaparib (10 μM) significantly suppressed the migration of keloid fibroblasts. Fibrosis markers in keloid fibroblasts significantly decreased after rucaparib treatment (20 μM). In patient-derived keloid xenograft model, rucaparib significantly reduced the size of keloid tissue. The study data suggest might be a novel therapeutic target for keloid disease. inhibitor, rucaparib, might be a promising therapeutic drug for the treatment of keloid disease.