Jing Huang1, Lili Zheng1, Hongfang Kong1, Fang Wang1, Yuan Su1, Hong Xin2. 1. Department of Obstetrics, The Second Hospital of Hebei Medical University, No. 215 Heping Xi Road, Shijiazhuang, 050000, Hebei, China. 2. Department of Obstetrics, The Second Hospital of Hebei Medical University, No. 215 Heping Xi Road, Shijiazhuang, 050000, Hebei, China. Electronic address: xh_hbyd@163.com.
Abstract
BACKGROUND: The biological functions of placental trophoblast cells have been reported to be critical in preeclampsia (PE) and its complications. Here, we aimed to investigate the role and underlying mechanism of soluble fms-like tyrsine kinase-1 (sFlt-1) and miR-139-5p in severe preeclampsia (sPE) by culturing the trophoblast cells from patients. METHODS: ELISA and qRT-PCR were used to measure the expression of sFlt-1 and miR-139-5p. The direct interaction between sFlt-1 and miR-139-5p was determined by luciferase reporter assay. Cell proliferation and invasion were evaluated by CCK-8 analysis and transwell assay. RESULTS: Our results showed that miR-139-5p was downregulated in sPE patients and was negatively correlated with the expression of sFlt-1. Further, sFlt-1 was a direct target of miR-139-5p, which monitored the expression of sFlt-1. Besides, miR-139-5p promoted the proliferation and invasion of trophoblast cells derived from sPE patients. Overexpression of sFlt-1 attenuated the effects of miR-139-5p on cell proliferation and invasion of trophoblast cells from sPE patients. CONCLUSION: Our research proposes a novel mechanism where the role of miR-139-5p is dependent on sFlt-1. Our data demonstrated that miR-139-5p promoted the proliferation and invasion of trophoblast cells by directly targeting sFlt-1 in PE.
BACKGROUND: The biological functions of placental trophoblast cells have been reported to be critical in preeclampsia (PE) and its complications. Here, we aimed to investigate the role and underlying mechanism of soluble fms-like tyrsine kinase-1 (sFlt-1) and miR-139-5p in severe preeclampsia (sPE) by culturing the trophoblast cells from patients. METHODS: ELISA and qRT-PCR were used to measure the expression of sFlt-1 and miR-139-5p. The direct interaction between sFlt-1 and miR-139-5p was determined by luciferase reporter assay. Cell proliferation and invasion were evaluated by CCK-8 analysis and transwell assay. RESULTS: Our results showed that miR-139-5p was downregulated in sPE patients and was negatively correlated with the expression of sFlt-1. Further, sFlt-1 was a direct target of miR-139-5p, which monitored the expression of sFlt-1. Besides, miR-139-5p promoted the proliferation and invasion of trophoblast cells derived from sPE patients. Overexpression of sFlt-1 attenuated the effects of miR-139-5p on cell proliferation and invasion of trophoblast cells from sPE patients. CONCLUSION: Our research proposes a novel mechanism where the role of miR-139-5p is dependent on sFlt-1. Our data demonstrated that miR-139-5p promoted the proliferation and invasion of trophoblast cells by directly targeting sFlt-1 in PE.