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Trichostatin A Induces NAG-1 Expression and Apoptosis in Human Endometriotic Stromal Cells
Seok Kyo Seo1,2, Jae Hoon Lee1,2, Seung Joo Chon3
11 Department of Obstetrics and Gynecology, Severance Hospital, Yonsei University College of Medicine, Seodaemun-gu, Seoul, Republic of Korea.
Abstract:
To investigate the effects of trichostatin A (TSA) on nonsteroidal anti-inflammatory drug-activated gene 1 (NAG-1) expression and apoptosis in human endometriotic stromal cells (HESCs), ectopic endometrial tissues were obtained from 15 patients with endometriotic cysts who underwent cystectomy. Human endometriotic stromal cells were isolated and cultured with different concentrations of TSA. Nonsteroidal anti-inflammatory drug-activated gene-1 messenger RNA (mRNA) and protein levels were evaluated by real-time polymerase chain reaction and Western blotting, respectively, and apoptosis was assessed by flow cytometry. Viability of HESCs was reduced in a dose-dependent manner by treatment with TSA. The percentage of early and late apoptotic HESCs was increased upon treatment with TSA. Nonsteroidal anti-inflammatory drug-activated gene-1 mRNA and protein expression was induced in a dose-dependent manner by TSA treatment. Gene knockdown experiments using small-interfering RNA confirmed an association between NAG-1 expression and TSA-induced apoptosis. Whether effects of TSA on NAG-1 gene expression are enhanced in the presence of 5-aza-2'-deoxycytidine (5-aza-dC) are also investigated; however, TSA-induced apoptosis was unaffected by 5-aza-dC. In conclusion, TSA induced apoptosis in HESCs via induction of NAG-1 expression. These results suggest that upregulation of NAG-1 contributes to TSA-induced apoptosis in HESCs.
Insights
Trichostatin A (TSA) induces apoptosis in human endometriotic stromal cells (HESCs) by upregulating nonsteroidal anti-inflammatory drug-activated gene 1 (NAG-1) expression. This suggests NAG-1 plays a key role in TSA-mediated cell death in endometriosis.
Area of Science:
- Endocrinology
- Molecular Biology
- Cell Biology
Background:
- Endometriosis is a condition characterized by ectopic endometrial tissue, leading to inflammation and pain.
- Nonsteroidal anti-inflammatory drug-activated gene 1 (NAG-1) is implicated in cellular stress responses and apoptosis.
- Trichostatin A (TSA) is a histone deacetylase inhibitor with potential therapeutic applications.
Purpose of the Study:
- To investigate the effect of TSA on NAG-1 expression and apoptosis in human endometriotic stromal cells (HESCs).
- To elucidate the role of NAG-1 in TSA-induced apoptosis in HESCs.
Main Methods:
- Human endometriotic stromal cells (HESCs) were isolated and treated with varying concentrations of TSA.
- NAG-1 mRNA and protein levels were quantified using real-time PCR and Western blotting.
- Apoptosis was assessed via flow cytometry; gene knockdown was performed using small-interfering RNA.
Main Results:
- TSA reduced HESC viability and increased apoptosis in a dose-dependent manner.
- TSA significantly induced NAG-1 mRNA and protein expression in HESCs.
- Gene knockdown of NAG-1 attenuated TSA-induced apoptosis, confirming its role.
Conclusions:
- TSA induces apoptosis in HESCs through the upregulation of NAG-1.
- NAG-1 is a critical mediator of TSA's pro-apoptotic effects in endometriosis.
- These findings highlight a potential therapeutic mechanism for endometriosis involving NAG-1 induction.
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