Mi RNA ‐320a inhibits trophoblast cell invasion by targeting estrogen‐related receptor‐gamma

Aim Micro RNA s (mi R s) play an essential role in the modulation of trophoblast function. We explored mi R ‐320a expression in the human placenta. In addition, we report the promising effect and target functional loop of mi R ‐320a in trophoblasts. Methods Mi R ‐320a expression was investigated in both pre‐eclamptic and healthy placenta tissues by quantitative real time‐polymerase chain reaction to determine how mi R ‐320a affected invasion, proliferation and migration in trophoblasts. A lipopolysaccharide ( LPS ) model was established in trophoblasts to reveal how LPS supplementation stimulated mi R ‐320a expression. Western blot was applied to measure protein expression, which was involved in pathways modulated by mi R ‐320a in pre‐eclamptic placentas. Results Mi R ‐320a expression was enhanced in the placental specimens of pre‐eclamptic patients. Excessive mi R ‐320a expression remarkably suppressed trophoblast invasion but did not affect migration or proliferation. However, transfection with mi R ‐320a inhibitor reinforced trophoblast invasion in vitro. Luciferase assays verified that estrogen‐related receptor‐gamma ( ERR γ) served as a direct target of mi R ‐320a. Quantitative real‐time polymerase chain reaction and Western blot demonstrated that excessive mi R ‐320a expression downregulated ERR γ transcription and translation. Additionally, LPS supplementation showed excessive mi R ‐320a expression and ERR γ downregulation. Impaired ERR γ and enhanced mi R ‐320a expression occurred in PE placentas compared to controls. Pearson correlation and linear regression analysis revealed that mi R ‐320a expression was negatively related to ERR γ expression in normal and pre‐eclamptic placentas. Conclusions These findings indicate that mi R ‐320a overexpression causes anomalous placentation by targeting ERR γ. Our research reveals the promising effect of mi R ‐320a and the ERR γ functional loop on placentation.