Am J Perinatol 2024; 41(03): 355-364
DOI: 10.1055/s-0041-1740300
Original Article

microRNA-203 Targets Insulin-Like Growth Factor Receptor 1 to Inhibit Trophoblast Vascular Remodeling to Augment Preeclampsia

Li Zhang
1   Department of Obstetrics, Maternal and Child health Hospital of Hubei Province, Wuhan City, Hubei Province, People's Republic of China
,
1   Department of Obstetrics, Maternal and Child health Hospital of Hubei Province, Wuhan City, Hubei Province, People's Republic of China
› Author Affiliations
Funding This research was supported by funds from the Hospital projects: Effects of L-arginine pamam-sirna-sflt1 nanocomposite on sflt1, PLDF and placental perfusion.

Abstract

Objective Preeclampsia (PE) is a pregnancy-specific condition featured by high blood pressure, edema, and proteinuria. Research about the role of microRNA (miR)-203 in PE remains insufficient. This experiment is designed to investigate the specific role of miR-203 in trophoblasts in PE.

Study Design miR-203 expression in placenta tissues of normal pregnant women and PE patients was examined to analyze the relevance between miR-203 and PE diagnostic efficiency and between miR-203 and blood pressure (systolic pressure and diastolic pressure) and proteinuria of PE patients. miR-203 expression was downregulated in hypoxia-cultured trophoblasts using miR-203 inhibitor to assess matrix metalloproteinase-9 (MMP-9) level. Then, the angiogenesis of trophoblasts with different treatments was determined. Subsequently, the target relation between miR-203 and insulin-like growth factor receptor 1 (IGF-1R) was predicted and verified. Additionally, the effect of IGF-1R in the mechanism of miR-203 modulating trophoblast vascular remodeling was detected.

Results miR-203 was overexpressed in the placenta of PE patients and it acted as a promising diagnostic indicator for PE. Moreover, miR-203 was positively associated with blood pressure (systolic pressure and diastolic pressure) and proteinuria of PE patients. miR-203 silencing in hypoxia-cultured trophoblasts enhanced trophoblast vascular remodeling. Mechanically, miR-203 bound to IGF-1R to suppress its transcription. IGF-1R downregulation counteracted the promotive effect of miR-203 silencing on trophoblast vascular remodeling.

Conclusion miR-203 was overexpressed in PE, and it targeted IGF-1R to limit trophoblast vascular remodeling.

Key Points

  • miR-203 is overexpressed in the placenta of PE patients.

  • miR-203 acts as a potential diagnostic marker for PE.

  • miR-203 targets IGF-1R to reduce trophoblast vascular remodeling in PE.

Ethical Approval

This study was approved and supervised by the ethics committee of Maternal and Child health Hospital of Hubei Province. All the patients signed the informed consent and they were informed with the object of this research. All procedures were strictly conducted in accordance with the code of ethics.


Authors' Contributions

All authors approved the final paper as submitted and agree to be accountable for all aspects of the work. L.Z. made substantial contributions to the conception of the present study. L.Z. and Y.L. performed the experiments and wrote the manuscript; Y.L. critically revised the paper.




Publication History

Received: 13 July 2021

Accepted: 24 October 2021

Article published online:
10 December 2021

© 2021. Thieme. All rights reserved.

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