Peroxisome proliferator-activated receptor gamma agonist suppresses human telomerase reverse transcriptase expression and aromatase activity in eutopic endometrial stromal cells from endometriosis.
10.5653/cerm.2013.40.2.67
- Author:
Hye Jin CHANG
1
;
Jae Hoon LEE
;
Kyung Joo HWANG
;
Mi Ran KIM
;
Jung Hyun YOO
Author Information
1. Health Promotion Center, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam, Korea.
- Publication Type:Original Article
- Keywords:
Endometriosis;
Peroxisome proliferator activated receptor gamma;
Rosiglitazone;
Human telomerase reverse transcriptase;
Aromatase;
Endometrium
- MeSH:
Aromatase;
Biopsy;
Biphenyl Compounds;
Blotting, Western;
Cell Proliferation;
Dinoprostone;
Down-Regulation;
Endometriosis;
Endometrium;
Female;
Humans;
Peroxisomes;
PPAR gamma;
Prostaglandin-Endoperoxide Synthases;
Stromal Cells;
Telomerase;
Thiazolidinediones
- From:Clinical and Experimental Reproductive Medicine
2013;40(2):67-75
- CountryRepublic of Korea
- Language:English
-
Abstract:
OBJECTIVE: To investigate the effect of peroxisome proliferator activated receptor gamma (PPARgamma) agonist on the cell proliferation properties and expression of human telomerase reverse transcriptase (hTERT) and aromatase in cultured endometrial stromal cell (ESC) from patients with endometriosis. METHODS: Human endometrial tissues were obtained from women with endometriosis and healthy women (controls) using endometrial biopsy. Isolated ESCs were cultured and the cell proliferation was measured by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide assay and expression of hTERT, aromatase, and cyclooxygenase (COX)-2 by western blotting according to the addition of rosiglitazone (PPARgamma agonist). RESULTS: We demonstrate that the cultured ESCs of endometriosis showed hTERT protein overexpression and increased cellular proliferation, which was inhibited by rosiglitazone, in a dose-dependent manner. At the same time, PPARgamma agonist also inhibited aromatase and COX-2 expression, resulting in decreased prostaglandin E2 production in the ESCs of endometriosis. CONCLUSION: This study suggests that PPARgamma agonist plays an inhibitory role in the proliferative properties of eutopic endometrium with endometriosis by down-regulation of hTERT and COX-2 expression; this could be a new treatment target for endometriosis.
