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In Vitro Assays to Evaluate the Migration, Invasion, and Proliferation of Immortalized Human First-trimester Trophoblast Cell Lines
Published on: March 5, 2019
Elevated microRNA-520g in pre-eclampsia inhibits migration and invasion of trophoblasts
Liansheng Jiang1, Anxiong Long1, Longyi Tan1
1Department of Clinical Laboratory, Shanghai First People's Hospital Baoshan Branch, Shanghai, PR China.
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.
Insights
Elevated first-trimester serum miR-520g levels indicate pre-eclampsia risk. This microRNA inhibits trophoblast migration and invasion by targeting MMP2, potentially contributing to pre-eclampsia.
Area of Science:
- Obstetrics and Gynecology
- Molecular Biology
- Biochemistry
Background:
- Pre-eclampsia (PE) is a severe obstetric complication linked to microRNA (miR) dysregulation.
- Understanding the role of specific microRNAs in PE pathophysiology is crucial for early detection and intervention.
Purpose of the Study:
- To investigate the role of microRNA-520g (miR-520g) in the development of severe pre-eclampsia.
- To characterize serum miR-520g levels and its cellular functions in trophoblast cells.
Main Methods:
- Serum samples from 19 severe pre-eclamptic and 19 normal pregnancies were analyzed using quantitative reverse transcription PCR (RT-qPCR).
- In situ hybridization localized miR-520g in placental trophoblasts.
- Transwell assays assessed trophoblast cell migration and invasion after miR-520g mimic treatment.
- Luciferase reporter assays identified miR-520g target genes.
Main Results:
- Serum miR-520g levels increased during pregnancy.
- First-trimester pre-eclampsia patients showed significantly higher serum miR-520g compared to controls.
- miR-520g was localized in the cytoplasm of early trimester placental trophoblasts.
- miR-520g mimic treatment inhibited trophoblast cell migration and invasion.
- Matrix metalloproteinase 2 (MMP2) was confirmed as a direct target of miR-520g.
Conclusions:
- Elevated first-trimester maternal serum miR-520g is associated with severe pre-eclampsia.
- miR-520g may contribute to pre-eclampsia by suppressing trophoblast migration and invasion, partly via MMP2 inhibition.
- This suggests miR-520g's role in defective spiral artery remodeling and PE pathogenesis.
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