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  • Title: Transforming growth factor (TGF)-beta1-induced human endometrial stromal cell decidualization through extracellular signal-regulated kinase and Smad activation in vitro: peroxisome proliferator-activated receptor gamma acts as a negative regulator of TGF-beta1.
    Author: Chang HJ, Lee JH, Hwang KJ, Kim MR, Chang KH, Park DW, Min CK.
    Journal: Fertil Steril; 2008 Oct; 90(4 Suppl):1357-65. PubMed ID: 18082740.
    Abstract:
    OBJECTIVE: To investigate the effect of transforming growth factor (TGF)-beta1 on the extracellular signal-regulated kinase (ERK) and Smad pathway and the role of peroxisome proliferator-activated receptor (PPAR)-gamma in cultured human endometrial stromal cells. DESIGN: Experimental study. SETTING: Infertility center of a tertiary university hospital. MATERIAL(S): Human endometrial tissues obtained by hysterectomy from patients with conditions other than endometrial diseases. INTERVENTION(S): Endometrial stromal cells were cultured under normal laboratory conditions. TGF-beta1, rosiglitazone (PPARgamma agonist), and PD98059 (ERK inhibitor) were added to endometrial stromal cell culture according to experimental purposes. MAIN OUTCOME MEASURE(S): Cell count, PRL expression, Smad and ERK phosphorylation, cyclooxygenase (COX)-2 expression, and prostaglandin E(2) (PGE(2)) release. RESULT(S): TGF-beta1 inhibited cellular proliferation and induced the expressions of COX-2, PGE(2), and PRL of cultured human endometrial stromal cells. These effects may be mediated by Smad and ERK phosphorylation. Treatment with rosiglitazone, a PPARgamma agonist, reversed the TGF-beta1 effect by antagonizing the activation of ERK and Smad that was induced by TGF-beta1. CONCLUSION(S): PPARgamma plays a negative role by directly acting on Smad and ERK phosphorylation in human endometrial cell decidualization that is induced by TGF-beta1 in vitro.
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