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CircYTHDF1/miR-19b-3p/YTHDF1 axis contributes to pregnancy-induced hypertension development by enhancing vascular
Fangyun Wang1, Qinping Yang1, Xiaolan Wang1
1Department of Obstetrics and Gynecology, Fuqing Maternal and Child Health Hospital, Fuqing, People's Republic of China.
Insights
This study reveals that circYTHDF1 exacerbates pregnancy-induced hypertension by promoting vascular endothelial cell injury. Targeting the circYTHDF1/miR-19b-3p/YTHDF1 axis offers a potential new treatment strategy for PIH.
Area of Science:
- Vascular Biology
- Molecular Mechanisms of Disease
- Reproductive Medicine
Background:
- Pregnancy-induced hypertension (PIH) is a significant complication of pregnancy with poorly understood mechanisms.
- CircRNAs, like circYTHDF1, are emerging as key players in various biological processes, but their role in PIH remains unclear.
Purpose of the Study:
- To elucidate the biological role and underlying mechanisms of circ_0004858 (circYTHDF1) in pregnancy-induced hypertension (PIH).
- To investigate the potential of the circYTHDF1/miR-19b-3p/YTHDF1 axis as a therapeutic target for PIH.
Main Methods:
- ELISA for inflammatory cytokines and biochemical parameters.
- Flow cytometry for cell apoptosis.
- Western blot and qRT-PCR for gene and protein expression analysis.
- Luciferase reporter assay to confirm molecular interactions.
Main Results:
- Elevated levels of inflammatory cytokines and Ang-II in PIH patients.
- circYTHDF1 and YTHDF1 were upregulated, while miR-19b-3p was downregulated in HUVECs under PIH conditions.
- circYTHDF1 promotes ferroptosis and apoptosis in vascular endothelial cells via the circYTHDF1/miR-19b-3p/YTHDF1 axis.
Conclusions:
- The circYTHDF1/miR-19b-3p/YTHDF1 axis plays a critical role in vascular endothelial cell injury in PIH.
- This study provides novel insights into PIH pathogenesis and suggests a potential new therapeutic strategy.
Objective:
The biological role of circ_0004858 (circYTHDF1) in pregnancy-induced hypertension (PIH) and the underlying mechanisms were unknown, and which were explored in this study.
Methods:
ELISA was employed to detect the level of inflammatory cytokines and biochemical parameters; flow cytometry was employed to detect cell apoptosis; western blot and qRT-PCR were employed to examine expression level.
Results:
The level of IL-1β, TNF-α, IL-6, TGF-β1, ET-1, and Ang-II were significantly elevated in the peripheral blood of PIH patients. The co-culture of HUVEC and CD4+ T cells isolated from the peripheral blood of PIH patients significantly elevated the apoptosis and expression level of NRF2/HO-1 but reduced the protein level of ferroptosis-related markers (GPX4, FSP, and CoQ10B) in HUVEC. Also, the expression of circYTHDF1 and YTHDF1 were markedly up-regulated in HUVEC co-cultured with CD4+ T cells isolated from PIH patients, but miR-19b-3p expression was markedly down-regulated, and the similar results were observed in Ang-II-treated HUVEC. Based on the predicted binding sites, the luciferase reporter assay confirmed the interaction between miR-19b-3p and circYTHDF1 or YTHDF1. The results of qRT-PCR and western blot further demonstrated that circYTHDF1 competitively bound to miR-19b-3p to up-regulate YTHDF1 in HUVEC. Functionally, deleting circYTHDF1markedly reduced ferroptosis and apoptosis in Ang-II-treated HUVEC, but both which were reversed by miR-19b-3p inhibitor, suggesting the involvement of circYTHDF1/miR-19b-3p/YTHDF1 axis in vascular endothelial cell injury in PIH.
Conclusions:
This study may provide a novel insight into the pathogenesis of PIH as well as a new treatment strategy.
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