Suppression of IL-1β-induced COX-2 expression by trichostatin A (TSA) in human endometrial stromal cells

ObjectiveOver-production of cyclooxygenase-2 (COX-2) plays an important role in the positive feedback loop that leads to proliferation and inflammation in endometriosis. Following our observation that histone deacetylase inhibitors (HDACIs) trichostatin A (TSA) and valproic acid (VPA) can suppress proliferation of endometrial stromal cells, we sought to determine whether TSA suppresses IL-1β-induced COX-2 expression in endometrial stromal cells.Study DesignIn vitro study using a recently established immortalized endometrial stromal cell line. The stromal cells were pretreated with TSA before stimulation with IL-1β, and COX-2 gene and protein expression was measured by real-time quantitative RT-PCR and Western blot analysis, respectively.ResultsIL-1β stimulated COX-2 expression in a concentration-dependent manner in endometrial stromal cells. The induced COX-2 gene and protein expression were suppressed by TSA pretreatment.ConclusionsTSA suppresses IL-1β-induced COX-2 gene and protein expression in endometrial stromal cells. This finding, coupled with the findings that TSA and another HDACI, valproic acid, suppress proliferation and induce cell cycle arrest, suggests that HDACIs are a promising class of compound that has therapeutic potential for endometriosis.