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Updated: Jul 17, 2026
Isolation of Human Endometrial Stromal Cells for In Vitro Decidualization
Published on: September 1, 2018
Suppression of IL-1beta-induced COX-2 expression by trichostatin A (TSA) in human endometrial stromal cells
1Department of Pediatrics, Medical College of Wisconsin, 8701 Watertown Plank Road, MS 756, Milwaukee, WI 53226-0509, USA.
Objective:
Over-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-1beta-induced COX-2 expression in endometrial stromal cells.
Study Design:
In vitro study using a recently established immortalized endometrial stromal cell line. The stromal cells were pretreated with TSA before stimulation with IL-1beta, and COX-2 gene and protein expression was measured by real-time quantitative RT-PCR and Western blot analysis, respectively.
Results:
IL-1beta 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.
Conclusions:
TSA suppresses IL-1beta-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.
Insights
Trichostatin A (TSA) suppresses cyclooxygenase-2 (COX-2) in endometriosis cells. This histone deacetylase inhibitor reduces inflammation and proliferation, showing potential as an endometriosis therapy.
Area of Science:
- Endocrinology
- Molecular Biology
- Cell Biology
Background:
- Cyclooxygenase-2 (COX-2) over-production drives inflammation and proliferation in endometriosis.
- Histone deacetylase inhibitors (HDACIs) like trichostatin A (TSA) and valproic acid (VPA) have shown promise in suppressing endometrial stromal cell proliferation.
Purpose of the Study:
- To investigate whether TSA can inhibit IL-1beta-induced COX-2 expression in endometrial stromal cells.
- To explore the therapeutic potential of HDACIs for endometriosis.
Main Methods:
- Utilized an in vitro immortalized human endometrial stromal cell line.
- Pretreated cells with TSA prior to IL-1beta stimulation.
- Quantified COX-2 gene and protein expression using real-time quantitative RT-PCR and Western blot analysis.
Main Results:
- IL-1beta significantly increased COX-2 expression in a dose-dependent manner.
- TSA pretreatment effectively suppressed both COX-2 gene and protein levels induced by IL-1beta.
- HDACIs TSA and VPA were previously shown to inhibit cell proliferation and induce cell cycle arrest.
Conclusions:
- TSA effectively suppresses IL-1beta-induced COX-2 expression at both gene and protein levels in endometrial stromal cells.
- HDACIs represent a promising therapeutic strategy for endometriosis due to their anti-proliferative and anti-inflammatory effects.
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