| Role of ERK (Extracellular Signal Regulated Kinas) and PPAR gamma(Peroxisome Proliferator-Activated Receptor Gamma) on TGF-beta1 Induced Human Endometrial Stromal Cell Decidualization. |
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Hye Jin Chang, Jae Hoon Lee, Mi Ran Kim, Kyung Joo Hwang, Dong Wook Park, Churl K Min |
1Department Molecular Science and Technology, School of Medicine, Ajou University, Suwon, Korea.
2Department of Obstetrics and Gynecology, School of Medicine, Ajou University, Suwon, Korea. |
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| Abstract |
OBJECTIVE
To investigate the role of ERK and PPAR gamma on the TGF-beta1 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-beta1 (5 ng/ml), Rosiglitazone (50 nM), and PD98059 (20 microgram) 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-beta1 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, PPAR gamma agonist, prevented TGF-beta1 effect on cell proliferation. Furthermore, Rosiglitazone inhibited TGF-beta1 induced activation of ERK, consequently reduced PGE2 and prolactin production. CONCLUSION: TGF-beta1 induced decidualization of endometrial stromal cell through Smad and ERK phosphorylation. PPAR gamma acts as a negative regulator of human endometrial cell decidualization in vitro. |
| Key Words:
Decidualization; TGF-beta1; PPAR gamma; ERK; Smad |
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