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.
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.
Authors: Xin Fang; Nan Ni; Yang Gao; John P Lydon; Ivan Ivanov; Monique Rijnkels; Kayla J Bayless; Qinglei Li Journal: Biol Reprod Date: 2020-12-01 Impact factor: 4.285
Authors: Nicole M Kane; Marius Jones; Jan J Brosens; Rodney W Kelly; Philippa T K Saunders; Hilary O D Critchley Journal: PLoS One Date: 2010-09-24 Impact factor: 3.240
Authors: Helena Rodriguez-Caro; Rebecca Dragovic; Mengni Shen; Eszter Dombi; Ginny Mounce; Kate Field; Jamie Meadows; Karen Turner; Daniel Lunn; Tim Child; Jennifer Helen Southcombe; Ingrid Granne Journal: J Extracell Vesicles Date: 2019-01-29