Aiping Qin1, Jinchun Qin2, Yufu Jin2, Wei Xie2, Li Fan3, Lingyun Jiang2, Fuhua Mo2. 1. Department of Reproductive Center, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, China. Electronic address: apqin2001@sina.com. 2. Department of Reproductive Center, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, China. 3. Department of Reproductive Center, Liuzhou Maternity and Child Healthcare Hospital, Liuzhou, Guangxi Zhuang Autonomous Region, China.
Abstract
OBJECTIVE: To investigate the effect of dehydroepiandrosterone (DHEA) on mouse decidual endometrial stromal cells (ESCs) and to explore mechanisms regulating endometrial receptivity. STUDY DESIGN: Mouse ESCs were incubated with increasing concentrations of DHEA during decidualization. Treatment with flutamide (FLU), a specific androgen receptor (AR) antagonist, was also performed. Flow cytometry was used to measure intracellular reactive oxygen species (ROS). Real time-PCR was used to determine mRNA expression of decidual PRL-related protein (dPRP), AR, and HomeoboxA10 (HOXA10). Protein levels of AR and HOXA10 were measured by western blot. RESULTS: DHEA significantly inhibited ESC proliferation at concentrations ≥1×10(-6)M. DHEA treatment reduced intracellular ROS in a dose-dependent manner. Expression of dPRP was minimally affected by DHEA at concentrations of 1 to 100nM. However, DHEA (100nM) significantly increased the expression of HOXA10 at both the mRNA and protein levels (P<0.01). Importantly, this DHEA-mediated increase in HOXA10 was attenuated by treatment with FLU. Finally, neither DHEA nor FLU influenced expression of AR mRNA or protein. CONCLUSION: Low concentration of DHEA improves the antioxidant capacity of decidual ESCs. DHEA treatment may also improve endometrium receptivity via AR.
OBJECTIVE: To investigate the effect of dehydroepiandrosterone (DHEA) on mouse decidual endometrial stromal cells (ESCs) and to explore mechanisms regulating endometrial receptivity. STUDY DESIGN:Mouse ESCs were incubated with increasing concentrations of DHEA during decidualization. Treatment with flutamide (FLU), a specific androgen receptor (AR) antagonist, was also performed. Flow cytometry was used to measure intracellular reactive oxygen species (ROS). Real time-PCR was used to determine mRNA expression of decidual PRL-related protein (dPRP), AR, and HomeoboxA10 (HOXA10). Protein levels of AR and HOXA10 were measured by western blot. RESULTS:DHEA significantly inhibited ESC proliferation at concentrations ≥1×10(-6)M. DHEA treatment reduced intracellular ROS in a dose-dependent manner. Expression of dPRP was minimally affected by DHEA at concentrations of 1 to 100nM. However, DHEA (100nM) significantly increased the expression of HOXA10 at both the mRNA and protein levels (P<0.01). Importantly, this DHEA-mediated increase in HOXA10 was attenuated by treatment with FLU. Finally, neither DHEA nor FLU influenced expression of AR mRNA or protein. CONCLUSION: Low concentration of DHEA improves the antioxidant capacity of decidual ESCs. DHEA treatment may also improve endometrium receptivity via AR.
Authors: Songhee Jeon; Quan Feng Liu; Hua Cai; Ha Jin Jeong; Su-Hyun Kim; Dong-Il Kim; Ju-Hee Lee Journal: Chin Med Date: 2020-10-20 Impact factor: 5.455
Authors: Önder Çelik; Mustafa Acet; Aytaç İmren; Nilüfer Çelik; Aynur Erşahin; Lebriz Hale Aktun; Barış Otlu; Sudenaz Çelik; Eray Çalışkan; Cihat Ünlü Journal: J Turk Ger Gynecol Assoc Date: 2017-12-15
Authors: Victoria L Boughton Nelson; Ariel L Negrón; Inefta Reid; Justin A Thomas; Leon Yang; Richard Z Lin; Maricedes Acosta-Martínez Journal: Biomed Res Int Date: 2017-03-05 Impact factor: 3.411
Authors: Douglas A Gibson; Ioannis Simitsidellis; Olympia Kelepouri; Hilary O D Critchley; Philippa T K Saunders Journal: Fertil Steril Date: 2018-02-15 Impact factor: 7.329