Liansheng Jiang1, Anxiong Long1, Longyi Tan1, Mao Hong1, Jingjing Wu2, Leiming Cai1, Qian Li3. 1. Department of Clinical Laboratory, Shanghai First People's Hospital Baoshan Branch, Shanghai, PR China. 2. Department of Obstetrics and Gynecology, Shanghai First People's Hospital Baoshan Branch, Shanghai, PR China. 3. Department of Clinical Laboratory, Shanghai First People's Hospital Baoshan Branch, Shanghai, PR China. Electronic address: aqianmerry@163.com.
Abstract
INTRODUCTION: Pre-eclampsia (PE) is a common and severe obstetric complication. MicroRNAs (miRs) have emerged as molecules that are associated with the disease. METHODS: Quantitative reverse transcription PCR (RT-qPCR) was used for serum miR-520g characterization from 19 severe pre-eclamptic and 19 normal pregnancies. In situ hybridation was adopted to localize microRNA-520g (miR-520g). Migration and invasion of HTR-8/SVneo cells were evaluated after miR-520g mimic treatment with transwell system. MiR-520g target gene was verified in luciferase reporter system. RESULTS: The expression of serum miR-520g displayed an upward trend as pregnancies progress. At first-trimester, miR-520g in pre-eclampsia was significantly higher than that in the control, but no significant differences were found in the second and last trimesters. MiR-520g localized in cytoplasm of early trimester placental trophoblasts. The migration and invasion of HTR8/SVneo were inhibited by miR-520g mimic treatment. Matrix metalloproteinase 2 (MMP2) was verified as a direct target of miR-520g. CONCLUSIONS: Elevated maternal serum level of miR-520g level in first trimester was detected in patients with severe PE. By suppressing the migration and invasion of trophoblast via at least partial inhibition of MMP2 translation inhibition, miR-520g might play a role in the defective spiral artery remodeling, and thus contribute to pre-eclampsia pathophysiology.
INTRODUCTION: Pre-eclampsia (PE) is a common and severe obstetric complication. MicroRNAs (miRs) have emerged as molecules that are associated with the disease. METHODS: Quantitative reverse transcription PCR (RT-qPCR) was used for serum miR-520g characterization from 19 severe pre-eclamptic and 19 normal pregnancies. In situ hybridation was adopted to localize microRNA-520g (miR-520g). Migration and invasion of HTR-8/SVneo cells were evaluated after miR-520g mimic treatment with transwell system. MiR-520g target gene was verified in luciferase reporter system. RESULTS: The expression of serum miR-520g displayed an upward trend as pregnancies progress. At first-trimester, miR-520g in pre-eclampsia was significantly higher than that in the control, but no significant differences were found in the second and last trimesters. MiR-520g localized in cytoplasm of early trimester placental trophoblasts. The migration and invasion of HTR8/SVneo were inhibited by miR-520g mimic treatment. Matrix metalloproteinase 2 (MMP2) was verified as a direct target of miR-520g. CONCLUSIONS: Elevated maternal serum level of miR-520g level in first trimester was detected in patients with severe PE. By suppressing the migration and invasion of trophoblast via at least partial inhibition of MMP2 translation inhibition, miR-520g might play a role in the defective spiral artery remodeling, and thus contribute to pre-eclampsia pathophysiology.
Authors: Lisa Levine; Andreas Habertheuer; Chirag Ram; Laxminarayana Korutla; Nadav Schwartz; Robert W Hu; Sanjana Reddy; Andrew Freas; Patrick D Zielinski; Joey Harmon; Sudheer Kumar Molugu; Samuel Parry; Prashanth Vallabhajosyula Journal: Sci Rep Date: 2020-04-14 Impact factor: 4.379