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KMID : 0358220060330020105
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Korean Journal of Fertility and Sterility
2006 Volume.33 No. 2 p.105 ~ p.113
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Role of ERK (Extracellular Signal Regulated Kinas) and PPARγ (Peroxisome Proliferator-Activated Receptor Gamma) on TGF-β1 Induced Human Endometrial Stromal Cell Decidualization
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Chang Hye-Jin
Lee Jae-Hoon
Kim Mi-Ran
Hwang Kyoung-Joo
Park Dong-Uk
Min Churl-K.
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Abstract
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Objective: To investigate the role of ERK and PPARγ on the TGF-β1 induced human endometrial stromal cell decidualization in vitro.
Method: Endometrial stromal cells are cultured under the following condition: DMEM/F12 (10% FBS, 1 nM E2 and 100 nM P4). TGF-β1 (5 ng/ml), Rosiglitazone (50 nM), and PD98059 (20 μM) were added according to experimental purposes. Trypan-Blue and hematocytometer were utilized to count cell number. Enzyme-linked immunosorbent assay (ELISA) and western blotting were utilized to detect proteins.
Result: TGF-β1 inhibited proliferation of cultured human endometrial stromal cells and induced expression of PGE2 and prolactin. This effect was mediated by Smad and ERK activation. Administration of rosiglitazone, PPARγ agonist,prevented TGF-β1 effect on cell proliferation. Furthermore, Rosiglitazone inhibited TGF-β1 induced activation of ERK, consequently reduced PGE2 and prolactin production.
Conclusion: TGF-β1 induced decidualization of endometrial stromal cell through Smad and ERK phosphorylation.
PPARγ acts as a negative regulator of human ndometrial cell decidualization in vitro.
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KEYWORD
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Decidualization, TGF-β1, PPARγ, ERK, Smad
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