Peroxisome proliferator-activated receptor γ agonist suppresses human telomerase reverse transcriptase expression and aromatase activity in eutopic endometrial stromal cells from endometriosis

To investigate the effect of peroxisome proliferator activated receptor γ (PPARγ) 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. Human endometrial...

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Published inClinical and experimental reproductive medicine Vol. 40; no. 2; pp. 67 - 75
Main Authors Chang, Hye Jin, Lee, Jae Hoon, Hwang, Kyung Joo, Kim, Mi Ran, Yoo, Jung Hyun
Format Journal Article
LanguageEnglish
Published Korea (South) The Korean Society for Reproductive Medicine 01.06.2013
대한생식의학회
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ISSN2233-8233
2233-8241
DOI10.5653/cerm.2013.40.2.67

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Summary:To investigate the effect of peroxisome proliferator activated receptor γ (PPARγ) 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. 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 (PPARγ agonist). 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, PPARγ agonist also inhibited aromatase and COX-2 expression, resulting in decreased prostaglandin E2 production in the ESCs of endometriosis. This study suggests that PPARγ 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.
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These authors contributed equally to this work.
G704-001601.2013.40.2.005
ISSN:2233-8233
2233-8241
DOI:10.5653/cerm.2013.40.2.67