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<p>Preeclampsia (PE) is a severe pregnancy complication that endangers maternal and fetal health. Accumulating evidence indicates that miR-126-3p is aberrantly expressed in PE placentas, yet its specific regulatory mechanism remains poorly defined. In the present study, we confirmed that miR-126-3p was significantly upregulated in placental tissues from PE patients. Functional assays demonstrated that overexpression of miR-126-3p suppressed proliferation, migration and invasion of HTR-8/SVneo trophoblast cells, and induced cell apoptosis, while miR-126-3p knockdown exerted opposite effects. Dual-luciferase reporter assay verified that miR-126-3p directly targeted PIK3R. Further mechanism experiments revealed that miR-126-3p inactivated the PI3K/AKT signaling pathway. Intervention with PI3K agonist and inhibitor further validated that miR-126-3p modulated trophoblast biological behaviors dependent on the PI3K/AKT pathway. In conclusion, elevated miR-126-3p contributes to the development and progression of PE via inhibiting the PI3K/AKT pathway through targeting PIK3R2. This work provides a novel molecular mechanism and potential therapeutic target for PE.</p>

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MiR-126-3p promotes the development and progression of preeclampsia through the inactivation of the PI3K/AKT pathway

  • 期刊论文

  • 发表日期：

    2026年7月22日

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  • Pingping Zhu,
  • Yanjun Hu,
  • Jiaying Shen,
  • Jianqiong Zheng,
  • Tingting Liao,
  • Yeping Wang

摘要

Preeclampsia (PE) is a severe pregnancy complication that endangers maternal and fetal health. Accumulating evidence indicates that miR-126-3p is aberrantly expressed in PE placentas, yet its specific regulatory mechanism remains poorly defined. In the present study, we confirmed that miR-126-3p was significantly upregulated in placental tissues from PE patients. Functional assays demonstrated that overexpression of miR-126-3p suppressed proliferation, migration and invasion of HTR-8/SVneo trophoblast cells, and induced cell apoptosis, while miR-126-3p knockdown exerted opposite effects. Dual-luciferase reporter assay verified that miR-126-3p directly targeted PIK3R. Further mechanism experiments revealed that miR-126-3p inactivated the PI3K/AKT signaling pathway. Intervention with PI3K agonist and inhibitor further validated that miR-126-3p modulated trophoblast biological behaviors dependent on the PI3K/AKT pathway. In conclusion, elevated miR-126-3p contributes to the development and progression of PE via inhibiting the PI3K/AKT pathway through targeting PIK3R2. This work provides a novel molecular mechanism and potential therapeutic target for PE.