Li Guo1, Yu Liu2, Ying Guo2, Yongkang Yang3, Biliang Chen4. 1. Department of Obstetrics and Gynecology, Xijing Hospital,the Military Medical University of PLA Airforce (Fourth Military Medical University), China; Department of Obstetrics, 215 Hospital of Shaanxi Nuclear Industry, China. 2. Department of Obstetrics and Gynecology, Xijing Hospital,the Military Medical University of PLA Airforce (Fourth Military Medical University), China. 3. Department of Obstetrics and Gynecology, the Second Affiliated Hospital of Shaanxi University of Chinese Medicine, China. Electronic address: LiGuo200720140520@163.com. 4. Department of Obstetrics and Gynecology, Xijing Hospital,the Military Medical University of PLA Airforce (Fourth Military Medical University), China. Electronic address: cblxjh@fmmu.edu.cn.
Abstract
INTRODUCTION: Preeclampsia (PE) is one of the leading causes of maternal and fetal mortality globally. The imbalance of trophoblast homeostasis is closely linked with the pathogenesis of PE. MicroRNA-423-5p (miR-423-5p) has been reported to be abnormally expressed in placenta and blood plasma of pregnant women with PE. In the present study, miR-423-5p expression in blood plasma of pregnant women with PE and healthy pregnant women was detected. Also, the roles and molecular mechanisms of miR-423-5p in the development of trophoblast cells were further investigated. METHODS: Expression of miR-423-5p and insulin like growth factor 2 mRNA binding protein 1 (IGF2BP1) mRNA was detected by RT-qPCR assay. Protein expression of IGF2BP1, Bcl-2 and Bax was determined using western blot assay. Cell migratory and invasive capacities were assessed by transwell migration and invasion assay. Cell apoptotic rate was determined using flow cytometry via the double-staining of Annexin V-FITC/Propidium Iodide. The interaction between miR-423-5p and IGF2BP1 was demonstrated by bioinformatics analysis and luciferase reporter assay. RESULTS: MiR-423-5p was highly expressed in blood plasma of pregnant women with PE. MiR-423-5p inhibited migration, invasion and proliferation as well as induced apoptosis in HTR-8/SVneo cells. Further investigation revealed that IGF2BP1 was a target of miR-423-5p. Moreover, IGF2BP1 overexpression promoted migration, invasion and proliferation, suppressed apoptosis, and weakened miR-423-5p function in HTR-8/SVneo cells. DISCUSSION: MiR-423-5p inhibited migration, invasion and proliferation as well as induced apoptosis by targeting IGF2BP1 in HTR-8/SVneo cells, presenting a novel molecular basis implicated in PE pathogenesis.
INTRODUCTION: Preeclampsia (PE) is one of the leading causes of maternal and fetal mortality globally. The imbalance of trophoblast homeostasis is closely linked with the pathogenesis of PE. MicroRNA-423-5p (miR-423-5p) has been reported to be abnormally expressed in placenta and blood plasma of pregnant women with PE. In the present study, miR-423-5p expression in blood plasma of pregnant women with PE and healthy pregnant women was detected. Also, the roles and molecular mechanisms of miR-423-5p in the development of trophoblast cells were further investigated. METHODS: Expression of miR-423-5p and insulin like growth factor 2 mRNA binding protein 1 (IGF2BP1) mRNA was detected by RT-qPCR assay. Protein expression of IGF2BP1, Bcl-2 and Bax was determined using western blot assay. Cell migratory and invasive capacities were assessed by transwell migration and invasion assay. Cell apoptotic rate was determined using flow cytometry via the double-staining of Annexin V-FITC/Propidium Iodide. The interaction between miR-423-5p and IGF2BP1 was demonstrated by bioinformatics analysis and luciferase reporter assay. RESULTS:MiR-423-5p was highly expressed in blood plasma of pregnant women with PE. MiR-423-5p inhibited migration, invasion and proliferation as well as induced apoptosis in HTR-8/SVneo cells. Further investigation revealed that IGF2BP1 was a target of miR-423-5p. Moreover, IGF2BP1 overexpression promoted migration, invasion and proliferation, suppressed apoptosis, and weakened miR-423-5p function in HTR-8/SVneo cells. DISCUSSION: MiR-423-5p inhibited migration, invasion and proliferation as well as induced apoptosis by targeting IGF2BP1 in HTR-8/SVneo cells, presenting a novel molecular basis implicated in PE pathogenesis.
Authors: Hoda Y Abdallah; Noura R Abdelhamid; Eman A Mohammed; Nehal Y AbdElWahab; Noha Z Tawfik; Amal H A Gomaa; Eman A Toraih; Alia Ellawindy Journal: Sci Rep Date: 2022-08-08 Impact factor: 4.996