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miR-24-3p regulation of retinol binding protein 4 in trophoblast biofunction and preeclampsia
Zhan Li1, Xiaoli Ru1, Shuzhen Wang1
1Department of Obstetrics and Gynecology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Insights
MicroRNA-24-3p targets retinol-binding protein 4 (RBP4) in preeclampsia (PE) development. High miR-24-3p expression reduces RBP4, impacting trophoblast cell invasion and proliferation in PE.
Area of Science:
- Reproductive biology
- Molecular genetics
- Biochemistry
Background:
- Preeclampsia (PE) is a major cause of maternal mortality.
- Reduced retinol-binding protein 4 (RBP4) levels are observed in PE patients.
- Previous studies suggest a link between RBP4 and microRNAs in PE.
Purpose of the Study:
- To investigate the regulatory role of microRNA-24-3p (miR-24-3p) on RBP4 expression in preeclampsia.
- To elucidate the mechanism of miR-24-3p targeting RBP4 in trophoblast cells.
Main Methods:
- Bioinformatics analysis and database investigation to identify miR-24-3p as an RBP4 target.
- Quantitative analysis of RBP4 and miR-24-3p expression in human PE placenta.
- In vitro studies using HTR-8/SVneo cells, including transfection, dual-luciferase reporter assay, Transwell invasion, and CCK8 assays.
Main Results:
- Database analysis confirmed RBP4 as a miR-24-3p target.
- PE placentas showed significantly reduced RBP4 and elevated miR-24-3p expression.
- miR-24-3p directly targets RBP4's 3'-untranslated region, inhibiting RBP4 expression in HTR-8/SVneo cells.
- Inhibition of miR-24-3p reversed the effects on RBP4, restoring HTR-8/SVneo cell invasion and proliferation.
Conclusions:
- miR-24-3p directly targets and downregulates RBP4 expression in the context of preeclampsia.
- This regulatory interaction plays a significant role in trophoblast dysfunction and PE pathogenesis.
- Findings offer new insights into the molecular mechanisms underlying preeclampsia.
Abstract:
Preeclampsia (PE) is a pregnancy-related disease and is the leading cause of overall maternal mortality and morbidity. Our previous studies have shown that the serum and placental levels of retinol-binding protein 4 (RBP4) in PE are reduced. Our previous bioinformatics analysis predicted that RBP4 is a target of the microRNA miRNA-24-3p. In this study, our database analysis also indicated that RBP4 is a miR-24-3p target. Compared with that of the normal placenta, the expression level of RBP4 in human PE placenta was significantly reduced, and miR-24-3p was highly expressed. In HTR-8/SVneo cells, transfection of exogenous miR-24-3p reduced RBP4 expression. A dual-luciferase reporter assay validated RBP4 as a direct target of miR-24-3p, indicating that it directly binds to the 3'-untranslated region of RBP4. This binding was reversed by a mutation in the microRNA-binding site. Transwell invasion experiments and CCK8 assay showed that inhibitory effect of miR-24-3p reduced RBP4 mediated HTR-8/SVneo cell invasion and proliferation. These data provide a new overarching perspective on the physiological role played by miR-24-3p in regulating RBP4 during trophoblast dysfunction and PE development.
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