Abstract
Preeclampsia (PE) harms a significant number of pregnant women and fetuses. However, because of its complex pathological mechanisms, there is no cure except for delivery. This study identified the impact and mechanisms of action of HOXB3 in PE. The behaviors of HTR-8/SVneo cells were analyzed using a cell counting kit-8, EdU, and transwell assays. The interaction between HOXB3 and Notch1 was assessed using a luciferase reporter and chromatin immunoprecipitation assays. Expression was measured by quantitative real-time polymerase chain reaction, western blotting, and immunofluorescence assays. Additionally, the function of HOXB3 was evaluated in an established rat model of PE. We found that HOXB3 was upregulated in PE. HOXB3 overexpression facilitated trophoblast cell proliferation, migration, and invasion. HOXB3 transcriptionally regulated Notch1 by binding to its promoter. Notch1 knockdown abrogated the functions of HOXB3 and the-catenin pathway in trophoblasts. Suppression of the Wnt/β-catenin pathway abrogated the effects of HOXB3. Additionally, HOXB3 alleviated the symptoms in PE rats. In conclusion, HOXB3 transcriptionally activated Notch1 expression and the-catenin pathway, promoting trophoblast cell proliferation, invasion, and migration, thereby alleviating PE progression. This study provides a novel approach for PE therapy.
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